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61 publications mentioning mmu-mir-98

Open access articles that are associated with the species Mus musculus and mention the gene name mir-98. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 397
Other miRNAs from this paper: hsa-mir-98
MiR-98 mimic down-regulated Sfrp4 mRNA level, while miR-98 inhibitor, Mecp2 expression vector, Mecp2 siRNA also inhibited Sfrp4 expression. [score:12]
We found that miR-98 over -expression suppressed Trpc3 expression, which was partially rehabilitated by up-regulation of Mecp2. [score:10]
When cells were co -transfected with miR-98 mimic and pMSCV-Mecp2, the mRNA level of Trpc3 were higher than transfection of miR-98 mimic (P < 0.01) and lower than transfection of pMSCV-Mecp2 (P < 0.01), implying that Trpc3 expression suppressed by miR-98 over -expression was partially rehabilitated by Mecp2 up-regulation. [score:10]
All these facts show that Mecp2 expression level is down-regulated in GDM tissues, while miR-98 expression level is visibly increased in GDM placental tissues, suggesting that miR-98 may execute its effects by targeting Mecp2 in GDM in vivo. [score:10]
MiR-98 regulates endogenous Mecp2 expression in vitroAlthough Mecp2 was identified as a target gene for miR-98, it was unknown whether miR-98 could regulate endogenous Mecp2 expression. [score:9]
Demethylation reduces the expression of miR-98In order to analyze the effect of demethylation on the expression of miR-98, DNA methylation inhibitor 5-aza was used to treat JEG-3 cells, and then the expression level of miR-98 was detected by qRT-PCR (Fig. 2A). [score:9]
However, the mRNA level of Trpc3 in cells co -transfected with miR-98 inhibitor and Mecp2 siRNA was significantly weakened compared with miR-98 inhibitor alone (P < 0.01) and strengthened compared with Mecp2 siRNA alone (P < 0.01), displaying that miR-98 low expression -mediated the up-regulation of Trpc3 was partially attenuated by Mecp2 knockdown (Fig. 8A). [score:9]
MiR-98 and Mecp2 regulate the protein expression of DNA methyltransferaseBecause miR-98 was involved in DNA methylation, we wondered whether miR-98 and its target gene would affect the protein expression of DNA methyltransferase or not (Fig. 7). [score:8]
These data indicates that miR-98 may suppress Mecp2 expression through binding to miR-98 responsive element in the 3′-UTR of Mecp2, and Mecp2 may be a direct target of miR-98. [score:8]
MiR-98 indirectly regulates the expression of Trpc3 by targeting Mecp2Previous studies have identified that canonical transient receptor potential 3 (Trpc3) and secreted frizzled-related protein 4 (Sfrp4), which play roles in T2DM, are the target genes of Mecp2 13 14. [score:8]
Compared with corresponding control, the level of MECP2 protein was significantly down-regulated by miR-98 mimic and up-regulated by miR-98 inhibitor (Fig. 5A). [score:8]
An online search of miR-98 targets by Targetscan, PicTar and miRanda provided a large number of putative miRNA targets. [score:7]
MiR-98 not only directly targets Mecp2, but also indirectly regulates the target gene of Mecp2. [score:7]
In order to analyze the effect of demethylation on the expression of miR-98, DNA methylation inhibitor 5-aza was used to treat JEG-3 cells, and then the expression level of miR-98 was detected by qRT-PCR (Fig. 2A). [score:7]
When miR-98 mimic or inhibitor was co -transfected with the recombinant vector Mecp2-pGL3, luciferase activity was reduced by the miR-98 mimic and enhanced by the miR-98 inhibitor, suggesting that Mecp2 may be the target gene of miR-98. [score:7]
These data further confirm that miR-98 not only directly targets Mecp2, but also regulates the endogenous MECP2 expression. [score:7]
Mecp2 is a direct target of miR-98To figure out the possible molecular mechanisms by which miR-98 may perform in DNA methylation, its target genes were researched. [score:6]
Up-regulation of miR-98 expression in placental tissues from patients with GDM. [score:6]
MiR-98 indirectly regulates the expression of Trpc3 by targeting Mecp2. [score:6]
Mecp2 was down-regulated in GDM placental tissuesThen it was unclear whether miR-98 executed its effects by targeting Mecp2 in GDM in vivo? [score:6]
To verify the endogenous effects of miR-98 expression dysregulation on Mecp2, JEG-3 cells were transfected with miR-98 mimic or inhibitor. [score:6]
Although Mecp2 was identified as a target gene for miR-98, it was unknown whether miR-98 could regulate endogenous Mecp2 expression. [score:6]
Up-regulation of miR-98 expression in placental tissues from patients with GDMThe distribution of miR-98 in GDM placental tissues and control tissues was determined by in situ hybridization (Fig. 1A). [score:6]
The miR-98 mimic, mimic control, miR-98 inhibitor, inhibitor control, scramble siRNA control and Mecp2 siRNA were synthesized by GenePharma (GenePharma Co. [score:5]
However, the protein level of TRPC3 in cells co -transfected with miR-98 inhibitor and Mecp2 siRNA was significantly weaker than transfected with miR-98 inhibitor alone (P < 0.05) and stronger than transfected with Mecp2 siRNA alone (P < 0.05). [score:5]
An online search of miR-98 targets by Targetscan, PicTar and miRanda found that there was a miR-98 responsive element in 3′-UTR of Mecp2, which was a highly conserved domain among different species. [score:5]
However, only 1 μM 5-aza significantly inhibited miR-98 expression (P < 0.01). [score:5]
The miR-98 indirectly regulates Trpc3 expression by Mecp2. [score:5]
MiR-98 knockdown promoted Trpc3 expression, which was partially attenuated by depleting Mecp2 expression. [score:5]
Then it was unknown whether miR-98 affected the expression of Mecp2 target genes? [score:5]
Because miR-98 was involved in DNA methylation, we wondered whether miR-98 and its target gene would affect the protein expression of DNA methyltransferase or not (Fig. 7). [score:5]
Therefore, miR-98 may indirectly regulate glucose up-take through targeting Mecp2-Trpc3 pathway. [score:5]
How to cite this article: Cao, J. -L. et al. Up-regulation of miR-98 and unravelling regulatory mechanisms in gestational diabetes mellitus. [score:5]
In vitro cell experiment was used to confirm the relationship between miR-98 and DNA methylation, and found that over -expression of miR-98 increased global DNA methylational level, and partially recovered the inhibition of DNA methylation induced by 5-azacytidine. [score:5]
The results indicated that 0.1, 0.5, 1 μM 5-aza inhibited the expression of miR-98 in a dose -dependent manner. [score:5]
Additionally, miR-98 inhibitor significantly promoted the expression of Trpc3 (P < 0.01). [score:5]
Up-regulation of miR-98 in the placental tissues from patients with GDM. [score:4]
Interestingly, DNA methylation inhibitor 5-azacytidine could decrease the miR-98 level in human choriocarcinoma cell line JEG-3. Emerging evidence indicates that GDM has epigenetic effects on genes through DNA methylation, with consequences on fetal growth and development 15. [score:4]
HEK-293T cells were co -transfected with mimic control, miR-98 mimic, inhibitor control or miR-98 inhibitor and Mecp2-pGL3 for dual-luciferase assay. [score:4]
Furthermore, the luciferase activity was significantly enhanced by the miR-98 inhibitor compared with inhibitor control (P < 0.01; Fig. 5B). [score:4]
Mecp2 is a direct target of miR-98. [score:4]
To further confirm the binding site, base mutation of miR-98 targeting site in 3′-UTR of Mecp2 (designated as MeCP2-pGL3-Mut) was also conducted. [score:4]
Additionally, over -expression of miR-98 reduced the protein and mRNA level of Mecp2 and knockdown of miR-98 enhanced the protein and mRNA level of Mecp2. [score:4]
The trend of miR-98 in four groups, including Y < 25, Y25~30, Y30~35 and Y > 35, is similar, suggesting that up-regulation of miR-98 may be associated with the occurrence of GDM. [score:4]
The prediction of the miR-98 target gene. [score:3]
Then it was unclear whether miR-98 executed its effects by targeting Mecp2 in GDM in vivo? [score:3]
Demethylation reduces the expression of miR-98. [score:3]
The expression levels of miR-98 in GDM group were markedly higher than that in control group in Y30~35 (P < 0.05) and Y > 35 (P < 0.05). [score:3]
Among them, we focused on Mecp2 for the following reasons: (1) Targetscan, PicTar and miRanda prediction showed that there was a miR-98 responsive element in 3′-UTR of Mecp2, which is a highly conserved domain among different species (Fig. 3A). [score:3]
There was no significant effect of miR-98 on Sfrp4 expression. [score:3]
The confirmation of the miR-98 target. [score:3]
These results imply that enhanced miR-98 expression may take part in the occurrence of GDM by Mecp2-Trpc3 pathway. [score:3]
The expression of miR-98 in the placental tissues from patients with GDM and normal pregnant women was detected by in situ hybridization using DIG-labeled LNA probes specific to miR-98 (A). [score:3]
To verify the relationship between miR-98 and DNA methylation, the global DNA methylation level in JEG-3 cells transfected by miR-98 mimic or inhibitor was estimated by the content of 5-methylcytosine (5-MeC) detected by cells immunohistochemistry (Fig. 2B). [score:3]
Additionally, the mRNA level of Mecp2 detected by qRT-PCR was significantly decreased by miR-98 mimic (P < 0.01) and increased by miR-98 inhibitor (P < 0.01). [score:3]
These facts show that enforced miR-98 expression promotes global DNA methylation level. [score:3]
HEK-293T cells were co -transfected with Mecp2-pGL3 and miR-98 mimic or inhibitor. [score:3]
In this study, we found that miR-98 was significantly up-regulated in placental tissues from GDM patients compared with that in normal controls. [score:3]
So, there was no distinct trend exhibiting the effects of miR-98 and Mecp2 on the expression of Sfrp4 (Fig. 8B). [score:3]
Global DNA methylation level in miR-98 mimic or inhibitor -treated cells with or without 5-aza was detected by immunohistochemistry and estimated by the content of global 5-meC (B). [score:3]
While in control group, there was only weak expression of miR-98 in placenta. [score:3]
These results indicate that miR-98 affects the binding of miR-98 and 3′-UTR of Mecp2, leading to the change of Mecp2 translation. [score:3]
Thus, an evident inverse relationship is showed between miR-98 and Mecp2 expression levels. [score:3]
MiR-98 and Mecp2 regulate the protein expression of DNA methyltransferase. [score:3]
In order to further confirm that miR-98 affected the expression of Trpc3, the protein level of TRPC3 was detected by western blot (Fig. 8C). [score:3]
MiR-98 regulates endogenous Mecp2 expression in vitro. [score:3]
To figure out the possible molecular mechanisms by which miR-98 may perform in DNA methylation, its target genes were researched. [score:3]
MiR-98 regulates Mecp2 expression in in vitro cell experiment. [score:3]
MiR-98 enhances the DNA methylation level in vitroTo verify the relationship between miR-98 and DNA methylation, the global DNA methylation level in JEG-3 cells transfected by miR-98 mimic or inhibitor was estimated by the content of 5-methylcytosine (5-MeC) detected by cells immunohistochemistry (Fig. 2B). [score:3]
Taken together, these results indicate that miR-98 executes functions in GDM partially by targeting Mecp2-Trpc3 pathway. [score:3]
DNMT1 protein level had a downward tendency in cells treated by miR-98 inhibitor and a obvious increase by Mecp2 siRNA (P < 0.05). [score:3]
The expression of miR-98 in the placental tissues was also detected by qRT-PCR (B). [score:3]
MiR-98 inhibitor markedly reduced the ratio of 5-MeC positive cells (P < 0.05). [score:2]
These results show that the mRNA and protein levels of endogenous Mecp2 are regulated by miR-98. [score:2]
These results show that miR-98 can positively regulate the global DNA methylation level. [score:2]
So we speculate that miR-98 may be able to regulate DNA mathylation in GDM. [score:2]
To generate 3′-UTR luciferase reporter, partial sequence of the 3′-UTR from Mecp2 were cloned into the downstream of the firefly luciferase gene in pGL3-Control Vector (Promega, Madison, WI, USA) using primers in Table 2. Mutating miR-98 target site in the 3′-UTR of Mecp2 was used as control. [score:2]
Mutation experiment further confirmed that the binding site in the 3′-UTR of Mecp2 was specific for miR-98. [score:2]
To validate whether Mecp2 was the indeed target gene of miR-98 or not, a human Mecp2 3′-UTR fragment containing wild-type was cloned into the downstream of the firefly luciferase reporter gene in the pGL3 control vector (designated as Mecp2-pGL3) for the dual-luciferase assay (Fig. 4A). [score:2]
MiR-98 inhibitor significantly enhanced TRPC3 protein level (P < 0.05). [score:2]
The overall expression trend of miR-98 in all placental tissues of GDM group was consistent with that in Y30~35 and Y > 35 age groups and significantly increased compared with control group (P < 0.05). [score:2]
Compared with the mimic control, the luciferase activity was significantly suppressed by the miR-98 mimic, (P < 0.01). [score:2]
Compared with miR-98 mimic, miR-98 inhibitor significantly enhanced Mecp2 mRNA level (P < 0.001; Fig. 5B). [score:2]
However, transfection of miR-98 mimic into 5-aza -treated cells significantly enhanced the ratio of 5-MeC positive cells (P < 0.01). [score:1]
These results imply that miR-98 is sensitive to occurrence of GDM. [score:1]
The miR-98 level was detected in JEG-3 cells treated with 5-aza by qRT-PCR (A). [score:1]
To our knowledge, this is the first study to examine the relationship between the presence of maternal GDM and miR-98. [score:1]
Mutating the binding site of miR-98 in the 3′-UTR of Mecp2 was used as control (Mecp2-pGL3-Mut). [score:1]
In different age groups, strong signals of miR-98 were found in GDM placental tissues. [score:1]
The effects of miR-98 (A) and Mecp2 (B) on the protein levels of DNA methyltransferase (DNMT1, DNMT3a and DNMT3b) were detected by western blot. [score:1]
The reverse transcription and quantitative PCR of miRNA were carried using special probes for miR-98 and U6 (Applied Biosystems, Foster City, CA, USA) with TaqMan MicroRNA Reverse Transcription Kit and Universal PCR Master Mix (Applied Biosystems, Foster City, CA, USA). [score:1]
MiR-98 mimic increased DNMT1 protein level (P < 0.05) and Mecp2 expression vector decreased DNMT1 protein level (P < 0.05) compared with corresponding control. [score:1]
These results suggest that miR-98 may be related with DNA methylation. [score:1]
The distribution of miR-98 in GDM placental tissues and control tissues was determined by in situ hybridization (Fig. 1A). [score:1]
When cells were co -transfected with miR-98 mimic and pMSCV-Mecp2, the protein level of TRPC3 was higher than transfection of miR-98 mimic lone (P < 0.05) and close to the control. [score:1]
Black arrows indicate hybridization signals and the positive signals of miR-98 are blue. [score:1]
Our findings demonstrate that miR-98 and its pathways in placental tissues are associated with GDM. [score:1]
The histogram represents the MODs of positive signals of miR-98 in placentas. [score:1]
However, miR-98 and Mecp2 had no significant effects on the protein levels of DNMT3a and DNMT3B. [score:1]
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[+] score: 348
On the contrary, however, miR-98 was also found to be significantly upregulated in gastric cancer [33], colon cancer [34], and small-cell lung cancer [35], and inhibited the expression of tumor suppressor gene FUS1 [35]. [score:10]
As we found that SALL4 was a direct target gene of miR-98, and was involved in the miR-98 -mediated malignant phenotypes in HCC in vitro, we speculated that the downregulation of miR-98 might contribute to the upregulation of SALL4 in HCC tissues. [score:10]
data indicated that that after miR-98 upregulation, the E-cadherin protein levels were increased, while the protein levels of N-cadherin, Fibronectin, vimentin were reduced in HepG2 and SMMC-7721 cells (Figure 4C-4D), indicating that the EMT is downregulated after overexpression of miR-98 in HCC cells. [score:9]
Accordingly, our data demonstrate that overexpression of SALL4 reversed the inhibitory effects of miR-98 on the malignant phenotypes of HCC cells, suggesting that the suppressive role of miR-98 in HCC is through inhibition of SALL4. [score:9]
To further confirm these findings, we examined the SALL4 expression in HCC tissues, and found that the SALL4 levels were reversely correlated with miR-98, supporting that downregulation of miR-98 may contribute to the upregulation of SALL4 in HCC. [score:9]
As miRs could inhibit the translation of their target genes [7], we further conducted western blot to examine the protein level of SALL4 in HepG2 and SMMC-7721 cells after overexpression of miR-98. [score:9]
As miR-98 was downregulated in HCC, we transfected HepG2 and SMMC-7721 cells with miR-98 mimic to upregulate its expression. [score:9]
MiR-98, belongs to the let-7/miR-98 family, acts as an oncogene or tumor suppressor in some human cancers through inhibiting the protein expression of its different target genes [15, 16]. [score:9]
For instance, miR-98 could suppress the growth and metastasis of oral squamous cell carcinoma by inhibiting the expression of IGF1R [17]. [score:7]
Some studies have demonstrated that miR-98 has suppressive effects on oral squamous cell carcinoma [17], non-small-cell lung cancer [18], glioma [31], and melanoma [19], and plays an inhibitory role in tumor angiogenesis and invasion by inhibition of ALK4 and MMP11 [32]. [score:7]
In the present study, we found that restoration of SALL4 reversed the suppressive effect of miR-98 on the proliferation, migration, invasion and EMT of HCC cells, suggesting that miR-98 plays a suppressive role in HCC via inhibition of SALL4. [score:7]
These findings suggest that the upregulation of SALL4 may be caused by the downregulation of miR-98 in HCC. [score:7]
In this study, overexpression of miR-98 significantly increased the expression of E-cadherin, while reduced the protein levels of N-cadherin, fibronectin and vimentin, indicating that EMT was inhibited. [score:7]
Overexpression of SALL4 eliminates the inhibitory effects of miR-98 on MMPs expression and EMT in HCC cells. [score:7]
To further study the regulatory role of miR-98 in HCC, two common HCC cell lines HepG2 and SMMC-7721 were transfected with miR-98 mimic to upregulate its expression. [score:7]
In summary, we reveals a tumor suppressive role of miR-98 in HCC, partly at least, via inhibition of SALL4, suggesting that the miR-98/SALL4 axis may become a promising therapeutic target for HCC treatment. [score:7]
We further identified SALL4 as a novel target gene of miR-98, and found that miR-98 could inhibit the protein expression of SALL4 in HCC cells. [score:7]
Moreover, low miR-98 expression was significantly associated with the tumor size, metastasis, portal vein tumor embolus, and poor overall survival, suggesting that downregulation of miR-98 is involved in the HCC progression, and miR-98 may become a potential predicator for the prognosis of patients with HCC. [score:6]
Pathak et al. found that the upregulated miR-98 was associated with colon cancer pathways and correlated with cyto- or chemokine expression [34]. [score:6]
In addition, MMP2 and MMP9, two key matrix metalloproteinases involved in tumor cell migration and invasion, were also downregulated after miR-98 overexpression in HepG2 and SMMC-7721 cells (Figure 4A-4B). [score:6]
Overexpression of SALL4 reverses the suppressive effects of miR-98 on HCC cells. [score:5]
All HCC patients involved in this study were divided into high miR-98 expression group and low miR-98 expression group, according to the mean value of the miR-98 level as the cutoff point. [score:5]
In the control group, all 5 mice died from the 53th to the 65th days after implantation; however, only 1 mouse died in the miR-98 group, indicating that overexpression of miR-98 protected nude mice from death caused by overexpression of miR-98 in HepG2 cells (Figure 10B). [score:5]
Li et al. showed that miR-98 inhibited melanoma metastasis through a negative feedback loop with its target gene IL-6 [19]. [score:5]
These findings further suggest that miR-98 inhibits the HCC growth by inhibition of SALL4. [score:5]
We then used TargetScan, PicTar, and miRanda to analyze the potential targets of miR-98. [score:5]
Taken together, our data demonstrate that miR-98 can inhibit the protein expression of SALL4 via binding to the 3′UTR of SALL4 in HCC cells. [score:5]
Restoration of miR-98 significantly suppressed the proliferation, migration and invasion of HepG2 and SMMC-7721 cell lines, suggesting that it may have inhibitory effect on HCC growth and metastasis. [score:5]
Ni et al. reported that miR-98 targeted ITGB3 to inhibit proliferation, migration, and invasion of non-small-cell lung cancer [18]. [score:5]
Overexpression of SALL4 attenuates the suppressive effects of miR-98 on HCC cell proliferation. [score:5]
Overexpression of SALL4 eliminates the inhibitory effects of miR-98 on HCC cell migration and invasion. [score:5]
In vivo study further showed that overexpression of miR-98 significantly inhibited the tumor growth of HCC cells in nude mice, and protected them from tumor -induced death. [score:5]
Accordingly, miR-98 plays a suppressive role in the regulation of cell proliferation, migration, invasion and EMT of HCC cells. [score:4]
SALL4 is a direct target gene of miR-98 in HCC cells. [score:4]
These findings suggest that downregulation of miR-98 may contribute to the malignant progression of HCC. [score:4]
SALL4 is upregulated in HCC and inversely correlated to miR-98 levels. [score:4]
MiR-98 -overexpressing HepG2 and SMMC-7721 cells were further transfected with pcDNA3.1-SALL4 plasmid to restore its expression. [score:4]
MiR-98 inhibits MMPs expression and epithelial-mesenchymal transition (EMT) in HCC cells. [score:4]
As shown in Figure 2C and 2D, overexpression of miR-98 significantly decreased the proliferation of HepG2 and SMMC-7721 cells. [score:3]
As indicated in Figure 1B, the HCC patients with low miR-98 levels had shorter survival time when compared with those with high miR-98 levels, which further suggests that downregulation of miR-98 may predicate poor prognosis of HCC patients. [score:3]
A, B. Real-time RT-PCR was conducted to determine the miR-98 expression. [score:3]
However, no statistically significant association of miR-98 expression was found with the age, gender, AFP, HBV infection, or cirrhosis (Table 1). [score:3]
MiR-98 is downregulated in HCC, associated with malignant progression and poor prognosis. [score:3]
Our data showed that the cell migration and invasion were downregulated in the miR-98 group compared to the control group (Figure 3A-3D). [score:3]
MiR-98 inhibits the growth of HCC in vivoFinally, the effect of miR-98 on HCC growth in vivo was studied. [score:3]
Association between miR-98 expression and clinicopathologic features of patients with hepatocellular carcinoma. [score:3]
As indicated in Figure 5A, SALL4 was a putative target gene of miR-98, and perfect base pairing was observed between the seed sequence of mature miR-98 and the 3′UTR of SALL4. [score:3]
The relative miR-98 expression was normalized to U6. [score:3]
Mutations of miR-98 binding sites were introduced by site-directed mutagenesis, which was then cloned into the downstream of the firefly luciferase coding region of pMIR-GLOTM Luciferase vector, named pMIR-Mut SALL4. [score:3]
To determine the effect of miR-98 on the tumorigenesis of HCC cells in vivo, nude mice were injected subcutaneously in the dorsal flank with 5×10 [6] HepG2 cells stably transfected with miR-98 -overexpressing plasmid. [score:3]
SALL4 is a target gene of miR-98 in HCC cells. [score:3]
E, F. was conducted to examine the protein expression of SALL4 in HepG2 and SMMC-7721 cells transfected with miR-98 mimic or scramble miR mimic. [score:3]
MiR-98 is downregulated in HCC. [score:3]
As SALL4 has been found to be an important oncogene in HCC [30], we speculated that SALL4 might be involved in miR-98 -mediated inhibition of the malignant phenotypes of HCC cells. [score:3]
Real-time RT-PCR data showed that the miR-98 level was significantly upregulated in the miR-98 group, when compared to the control group (Figure 10A). [score:3]
To verify this speculation, we then conducted real-time RT-PCR to examine the SALL4 expression in HCC tissues and ANTs, and analyzed the correlation between the miR-98 and SALL4 levels in HCC tissues. [score:3]
After that, nude mice were subcutaneously implanted with HepG2 cells stably overexpressing miR-98. [score:3]
MiR-98 inhibits migration and invasion of HCC cells. [score:2]
We found that the protein expression of SALL4 was significantly decreased in the miR-98 group compared to the miR-NC group (Figure 5E and 5F). [score:2]
MiR-98 inhibits proliferation, migration, invasion and EMT of HCC cells. [score:2]
MiR-98 inhibits the growth of HCC in vivo. [score:2]
Future studies should further investigate the upstream regulatory mechanism underlying miR-98 expression as well as the downstream signaling pathways of SALL4 in HCC cells, which may help expand the understanding of miR-98/SALL4 axis in HCC. [score:2]
MiR-98 suppresses HCC cell proliferation. [score:2]
Deregulations of MiR-98 participate in the development and progression of some cancers [15, 19]. [score:2]
Besides, the E-cadherin protein levels were reduced, while the Fibronectin, N-cadherin and vimentin protein levels were increased in the miR-98+SALL4 group compared to the miR-98 group (Figure 8C-8D), suggesting that the EMT was promoted after restoration of SALL4 expression in HCC cells. [score:2]
These findings indicate that miR-98 can directly bind to seed sequence in the 3′UTR of SALL4. [score:2]
Figure 8HepG2 and SMMC-7721 cells were transfected with miR-98 mimic, or co -transfected with miR-98 mimic and SALL4 plasmid, respectively. [score:1]
HepG2 cells were then stably transfected with pYr-LVX-miR-98 lentiviral plasmid or blank pLVX-IRES-ZsGreen1 vector as controls. [score:1]
Figure 10 A. HepG2 cells were stably transfected with the blank pLVX-IRES-ZsGreen1 vector as Control or pYr-LVX-miR-98 lentiviral plasmid, and real-time RT-PCR was conducted to examine the miR-98 level in each group. [score:1]
B. Nude mice were subcutaneously implanted with HepG2 cells stably transfected with pYr-LVX-miR-98 lentiviral plasmid or blank pLVX-IRES-ZsGreen1 vector, respectively. [score:1]
HepG2 and SMMC-7721 cells were transfected with miR-98 mimic, or co -transfected with miR-98 mimic and SALL4 plasmid, respectively. [score:1]
Figure 4HCC HepG2 and SMMC-7721 cells transfected with miR-98 mimic or scramble miR mimic (miR-NC). [score:1]
However, co-transfection with MT-SALL4-3′UTR plasmid and miR-98 mimic had not effect on the luciferase activity (Figure 5C and 5D). [score:1]
Figure 5 A. The seed sequences of miR-98 in the wild type and mutant type 3′UTR of SALL4 are indicated. [score:1]
Finally, the effect of miR-98 on HCC growth in vivo was studied. [score:1]
C, D. The luciferase activity was notably decreased in HCC HepG2 and SMMC-7721 cells co -transfected with miR-98 mimics and WT-SALL4-3′UTR reporter plasmid, but unaltered in HepG2 and SMMC-7721 cells co -transfected with miR-98 mimics and MT-SALL4-3′UTR plasmid. [score:1]
The miR-98 was cloned into the pLVX-IRES-ZsGreen1 vector (Amspring) to construct the pYr-LVX-miR-98 lentiviral plasmid. [score:1]
Figure 7HepG2 and SMMC-7721 cells were transfected with miR-98 mimic, or co -transfected with miR-98 mimic and SALL4 plasmid, respectively. [score:1]
A. Real-time qPCR was conducted to determine the miR-98 levels in a total of 144 primary HCC tissues and matched adjacent normal tissues (ANTs). [score:1]
A. The seed sequences of miR-98 in the wild type and mutant type 3′UTR of SALL4 are indicated. [score:1]
The pcDNA3.1-SALL4 plasmid, miR-98 mimic, scramble miR mimic, were purchased from Amspring (Changsha, China). [score:1]
MiR-98 was cloned into the pLVX-IRES-ZsGreen1 lentiviral vector, generating the pYr-LVX-miR-98 plasmid, which was stably transfected into HepG2 cells. [score:1]
We then investigated the association between the miR-98 expression and the clinicopathological features of HCC. [score:1]
As indicated in Table 1, 88 cases (61.1%) were in the low miR-98 level group, while 56 cases (38.9%) were in high miR-98 level group. [score:1]
miR-98. [score:1]
Thus, the cancer-specific miR-98 may exert anti-tumor or oncogenic effects, depending on the cancer type. [score:1]
B. An inverse correlation was observed between the miR-98 and SALL4 mRNA levels in HCC tissues. [score:1]
Moreover, the decreased miR-98 levels were significantly associated with tumor size, metastasis, and portal vein tumor embolus (Table 1). [score:1]
Figure 1, associated with malignant progression and poor prognosis A. Real-time qPCR was conducted to determine the miR-98 levels in a total of 144 primary HCC tissues and matched adjacent normal tissues (ANTs). [score:1]
As indicated in Figure 3C, co-transfection with WT-SALL4-3′UTR plasmid and miR-98 mimic led to a significant decrease in the luciferase activity. [score:1]
To reveal the role of miR-98 in HCC, real-time RT-PCR was performed to examine the miR-98 levels in a total of 144 HCC tissues and ANTs. [score:1]
Figure 6HepG2 and SMMC-7721 cells were transfected with miR-98 mimic, or co -transfected with miR-98 mimic and SALL4 plasmid, respectively. [score:1]
Moreover, we found that the SALL4 levels were reversely correlated to the miR-98 levels in HCC tissues (Figure 9B). [score:1]
Figure 3HCC HepG2 and SMMC-7721 cells transfected with miR-98 mimic or scramble miR mimic (miR-NC). [score:1]
HCC HepG2 and SMMC-7721 cells transfected with miR-98 mimic or scramble miR mimic (miR-NC). [score:1]
Figure 2HCC HepG2 and SMMC-7721 cells transfected with miR-98 mimic or scramble miR mimic (miR-NC). [score:1]
SALL4 is reversely correlated with miR-98 in HCC. [score:1]
However, the exact role of miR-98 in the progression of HCC as well as the underlying mechanism still remains to be fully uncovered. [score:1]
Recently, Lin-28B, a RNA -binding protein, was suggested to promote tumor formation and invasion in HCC through coordinated repression of the let-7/miR-98 family and induction of multiple oncogenic pathways [20]. [score:1]
Cells were seeded into 24-well plates and co -transfected with 200 ng of pMIR-SALL4 or pMIR-SALL4-Mut vector and 100 ng of miR-98 mimic or scramble miR mimic, and the pRL-TK plasmid (Promega, Madison, WI) as internal normalization. [score:1]
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[+] score: 298
Figure 4MiR-98 overexpression inhibits the expression of Fas and caspase-3. (A) and (B) MiR-98 overexpression significantly prevented upregulation of Fas mRNA and protein level in H [2]O [2] -treated NRVCs. [score:11]
MiR-98 overexpression suppresses H [2]O [2] -induced upregulation of Fas and caspase-3 in cardiomyocytesWe next aimed to explore the underlying mechanism that miR-98 inhibited H [2]O [2] -induced apoptosis. [score:10]
n = 6. (B) Bcl-2 expression was suppressed by H [2]O [2] but upregulated by miR-98. [score:8]
MiR-98 overexpression suppresses H [2]O [2] -induced upregulation of Fas and caspase-3 in cardiomyocytes. [score:7]
As shown in Fig.   4A, compared with control group, Fas mRNA expression was significantly upregulated in the H [2]O [2] -treated NRVCs, which could be reversed by miR-98 overexpression. [score:7]
As Fas and caspase-3 were proved to be the target genes of miR-98 17, 18, we further verified the expression of Fas and caspase-3 in the presence of miR-98 overexpression. [score:7]
MiR-98 overexpression led to the decreased Fas protein expression in posttranscriptional level (Fig.   4B), further indicating that Fas was the target gene of miR-98. [score:7]
miR-98 overexpression significantly inhibited luciferase activity in the wild-type group, demonstrating that miR-98 could target at 3′-UTR of Fas (Fig.   5B). [score:7]
Meanwhile, miR-98 overexpression also reduced the upregulation of caspase-3 mRNA induced by H [2]O [2] (Fig.   4C). [score:6]
NRVCs were transfected with NC (negative control), miR-98 mimic (miR-98 mim), miR-98 inhibitor (miR-98 inh), and miR-98 mimic + inhibitor (miR-98 mim&inh) and then treated with H [2]O [2] (100 μM) for 4 h. (A) MTT assay suggested that miR-98 mimic restored cell viability of NRVCs treated with 100 μM H [2]O [2] for 4 h. n = 8. (B) Statistical results of TUNEL -positive cells per field indicated that miR-98 mimic suppressed H [2]O [2] treatment -induced cell apoptosis. [score:6]
In addition, miR-98 was verified to target Fas directly and regulated Fas -mediated apoptosis in HeLa cells [18]. [score:5]
Yang Y Ago T Zhai P Ab dellatif M Sadoshima J Thioredoxin 1 negatively regulates angiotensin II -induced cardiac hypertrophy through upregulation of miR-98/let-7Circ Res. [score:5]
n = 5. (C) and (D) The mRNA and protein expression of caspase-3 were also remarkably elevated by H [2]O [2] but reduced by miR-98 overexpression. [score:5]
The current results showed that overexpression of miR-98 reversed the reduction in Bcl-2 expression caused by acute ischemia, suggesting that Bcl-2 is involved in miR-98 -induced cardioprotection. [score:5]
Also, Bcl-2 expression was elevated in NRVCs after miR-98 overexpression (Fig.   3B). [score:5]
Fas and caspase-3 expression were also involved in this research because they were the key modulators of apoptosis and can be regulated by miR-98 17, 18. [score:4]
Yuan Y MicroRNA-98 and microRNA-214 post-transcriptionally regulate enhancer of zeste homolog 2 and inhibit migration and invasion in human esophageal squamous cell carcinomaMol Cancer. [score:4]
However, miR-98 overexpression induced a sharp decrease of Bax expression in NRVCs compared with NC group (Fig.   3A). [score:4]
Our work demonstrated that miR-98 was upregulated in MI mice and in oxidative stress-stimulated cardiomyocytes. [score:4]
However, the mechanism by which miR-98 reduced the apoptosis of cardiomyocytes through targeting Fas/Caspase-3 and simultaneously regulating mitochondrial apoptotic pathway remains to be elucidated. [score:4]
In addition, miR-98 targeted at the ACUACCUC sequence in the 3′-UTR of Fas mRNA directly to reduce Fas protein production. [score:4]
Overexpression of miR-98 attenuated the deterioration of left ventricular performance, as indicated by the increased EF and FS (Fig.   7C–E). [score:3]
n = 3. (C) miR-98 expression level in NRVCs after miR-98 mimic transfection. [score:3]
Recently, altered miR-98 expression has been found in several carcinomas [14]. [score:3]
Figure 2Overexpression of miR-98 prevents cardiomyocyte apoptosis in response to H [2]O [2]. [score:3]
n = 5. (E) MiR-98 significantly prevented upregulation of Fas mRNA level in the infarcted and border zones of MI mice. [score:3]
Real-time PCR analysis revealed that the expression of miR-98 in the infarcted and border zones of rat hearts at 3 days after MI was much lower than that in sham-operated animals (Fig.   1B). [score:3]
Meanwhile, we also examined the expression of miR-98 in heart tissues after MI for 3 days. [score:3]
Figure 3Effect of miR-98 on Bax and Bcl-2 expression and mitochondrial membrane potential (Δψm). [score:3]
As shown in Fig.   1D, 1, 2 and 3 days after injection of miR-98 agomir using our delivery method, miR-98 expression was markedly increased in the heart tissue. [score:3]
Real-time PCR analysis revealed that Fas mRNA levels were markedly increased in infarcted and border zones and the existence of miR-98 agomir led to the decreased expression of Fas in transcriptional level (Fig.   6E). [score:3]
At the same time, miR-98 significantly reversed the expression of Fas protein. [score:3]
However, H [2]O [2] -induced increase in monomeric form cells was reduced by miR-98 overexpression (Fig.   3C and D). [score:3]
Taken together, these results proved that miR-98 overexpression prevented H [2]O [2] -induced cardiomyocyte apoptosis and promoted cell survival. [score:3]
Western blot showed that the expression caspase-3 was significantly decreased by miR-98. [score:3]
Then, we overexpressed miR-98 in NRVCs by miR-98 mimic transfection and in mice hearts by miR-98 agomir injection. [score:3]
Figure 5Fas was the target gene of miR-98. [score:3]
Therefore, Fas was proved to be the target gene of miR-98. [score:3]
Cardiomyocytes were starved in serum-free medium for 24 hours, and then transiently transfected with miR-98 mimic (50 nM), miR-98 inhibitor (100 nM) and NC (50 nM), using X-treme GENE siRNA transfection reagent (Roche, Penzberg Germany) according to the manufacturer’s instructions. [score:3]
Overexpression of miR-98 decreases infarct size and improves cardiac function of infarcted heart in mice. [score:3]
Our findings suggest that miR-98 may provide a potential novel therapeutic approach for the treatment of ischemic heart disease. [score:3]
MiR-98 is downregulated in response to myocardial ischemic injury. [score:3]
Overexpression of miR-98 attenuated apoptosis in H [2]O [2] -treated NRVCs and MI mice mo del. [score:3]
MiR-98 overexpression prevented H [2]O [2] -induced cardiomyocyte apoptosisBased on the above results, we subsequently aimed to evaluate the effects of miR-98 overexpression on cell apoptosis. [score:3]
Moreover, overexpression of miR-98 also increased cell viability and prevented cell necrosis in H [2]O [2] -treated NRVCs (Fig.   2F and G). [score:3]
This reveals that overexpression of miR-98 during the infarct period might be a useful approach for heart protection. [score:3]
We next aimed to explore the underlying mechanism that miR-98 inhibited H [2]O [2] -induced apoptosis. [score:3]
Due to the non-homology of Fas in different species, we used computational methods to search for the potential targets of miR-98 in rats and constructed luciferase reporter plasmids containing the 3′-UTR of Fas. [score:3]
Firstly, the expression of miR-98 was detected in H [2]O [2] -treated cardiomyocytes and postinfarct cardiac tissues. [score:3]
In total, the present study demonstrates that miR-98 suppresses the apoptosis of cardiomyocytes, reduces the MI size, and improves the cardiac function. [score:3]
n = 6. (D) miR-98 expression level in rat ventricles after administration with miR-98 agomir. [score:3]
By contrast, the number of JC-1 monomeric cells was markedly reduced in NRVCs overexpressed miR-98. [score:3]
Li H miR-98 protects endothelial cells against hypoxia/reoxygenation induced-apoptosis by targeting caspase-3Biochem Biophys Res Commun. [score:3]
Furthermore, the effect of miR-98 mimic on H [2]O [2] -induced cell apoptosis was abolished by co-transfection with miR-98 inhibitor (Fig.   2D and E). [score:3]
Effect of miR-98 overexpression on ischemia -induced cardiomyocyte apoptosis. [score:3]
MiR-98 overexpression regulates apoptosis-related proteins and mitochondrial membrane potential. [score:3]
Furthermore, it was observed that the number of TUNEL -positive cells was significantly increased in H [2]O [2] group, which was diminished by miR-98 mimic but not by NC or miR-98 inhibitor (Fig.   2B and C). [score:3]
Moreover, miR-98 has been reported to be a sensitive marker of renal ischemic injury [16] and protect endothelial cells against hypoxia/reoxygenation induced-apoptosis by targeting caspase-3 [17]. [score:3]
MiR-98 -mimic, miR-98 inhibitor and NC were synthesized by Guangzhou RiboBio (Guangzhou, China). [score:3]
MiR-98 directly targets at the 3′-UTR of Fas. [score:3]
Fas and caspase-3 were identified to be the target genes of miR-98 in humans 17, 18 and the predicted site in caspase-3 3′-UTR showed a good conservative character among different species [17]. [score:3]
The cardioprotective effect of miR-98 was achieved by regulating Fas/Caspase-3 apoptotic signal pathway. [score:2]
MiR-98 overexpression markedly decreased the relative luciferase activity in the WT 3′-UTR but not mutant 3′-UTR of Fas mRNA. [score:2]
In contrast, compared with miRNA negative control (NC) transfection group, miR-98 overexpression by transfecting with miR-98 mimic significantly increased the cell viability of NRVCs treated with H [2]O [2] (Fig.   2A). [score:2]
As shown in Fig.   1A, compared with control group, miR-98 expression was significantly decreased by exposure to 100 μM H [2]O [2] in NRVCs. [score:2]
In this study, we found that Fas and caspase-3 were negatively regulated by miR-98. [score:2]
MiR-98 overexpression prevented H [2]O [2] -induced cardiomyocyte apoptosis. [score:2]
Consequently, we acknowledged from this study that miR-98 could negatively regulate MI injury -induced cell apoptosis possibly through Fas and caspase-3 pathway. [score:2]
Since miR-98 promoted cell survival and prevented cardiomyocyte apoptosis, we further investigated its role in regulating the expression of apoptosis-related proteins and mitochondrial membrane potential (Δψm ). [score:2]
n = 5. (F) MiR-98 suppressed the elevation of caspase-3 mRNA level in the infarcted, border and remote zones of MI mice. [score:2]
Wang S Let-7/miR-98 regulate Fas and Fas -mediated apoptosisGenes Immun. [score:2]
MiR-98 is one of the members of the let-7 miRNA family, which is first discovered to control the developmental timing of cell differentiation and proliferation in C. elegans 12, 13. [score:2]
Figure 7Reduction of infarct size and improvement of cardiac function by miR-98 in MI mice. [score:1]
We then tried to clarify whether antiapoptotic effects of miR-98 on cultured cells under H [2]O [2] conditions also exist under in vivo conditions in MI. [score:1]
Moreover, the activity of serum lactate dehydrogenase (LDH) (a marker for cardiac injury) increased obviously after MI, which was significantly attenuated by miR-98 agomir as well (Fig.   6C). [score:1]
The ascending aortic artery and the main pulmonary artery were clamped; then, miR-98 agomir (200 nmol·kg [−1] at the volume of 80 μL) was injected into the left ventricular cavity through the tip of the heart with a 30-gauge syringe. [score:1]
The levels of miR-98, caspase-3 and Fas mRNA were determined using SYBR Green incorporation on Roche Light-Cycler 480 Real Time PCR system (Roche, Germany), with U6 as an internal control for miR-98 and GAPDH for caspase-3 and Fas. [score:1]
Therefore, we have demonstrated for the first time that miR-98 protects against H [2]O [2] -induced mitochondrial dysfunction in NRVCs. [score:1]
The protein level of caspase-3 after miR-98 mimic transfection showed the similar trend with the mRNA level (Fig.   4D). [score:1]
Therefore, let-7/miR-98 miRNAs are considered as an oncomir family crucial in regulating cell cycle and apoptosis [15]. [score:1]
As expected, this elevation of caspase-3 activity was blocked by miR-98 agomir administration. [score:1]
Firstly, to investigate the effects of miR-98 on mitochondrial protection, we analyzed the expression of Bcl-2 and Bax and the mitochondrial membrane potential (Δψm). [score:1]
Consequently, miR-98 could reverse the H [2]O [2] induced elevation of Fas and caspase-3, and thus provide protections against ischemia -induced cardiomyocyte apoptosis. [score:1]
We found that the apoptosis percentage was increased by H [2]O [2] treatment, which was significantly diminished by miR-98 mimic (Figure 2 D and E). [score:1]
n = 6. (C) Serum lactate dehydrogenase (LDH) activity is increased in MI mice and restored by miR-98 agomir administration. [score:1]
However, miR-98 failed to affect the luciferase activity elicited by the construct carrying the Fas 3′-UTR with the mutant miR-98 -binding site (Fig.   5C). [score:1]
MI Mo del and Administration of miR-98 agomir. [score:1]
To determine the change of miR-98 in the different areas of infarcted hearts, miRNAs were isolated from infarcted zone, border zone and remote zone. [score:1]
The miR-98 agomirs (Ribo-bio, Guangzhou, China) are double-stranded RNA analogues identical to the mature mmu-miR-98–5p (5′-UGAGGUAGUAAGUUGUAUUGUU-3′). [score:1]
Meanwhile, miR-98 reduced the activation of Bax. [score:1]
Therefore, we speculated that miR-98 simultaneously modulated of the intrinsic and extrinsic pathways of myocardial apoptosis in MI. [score:1]
We then transfected HEK293T cells with the luciferase vector containing a wild-type or mutant miR-98 response element. [score:1]
The binding sites of miR-98 in the 3′-UTR of wild-type Fas mRNA were displayed, but mutant mRNA had few binding sites (Fig.   5A). [score:1]
n = 6. (D) Caspase-3 activity is promoted in MI mice and reversed by miR-98 agomir. [score:1]
In addition, flow cytometry was utilized to validate the protective role of miR-98 in H [2]O [2] -induced cardiomyocyte apoptosis. [score:1]
Then, HEK293T cells were seeded in a 96-well plate and co -transfected with 0.5 μg plasmid and miR-98 mimics or negative controls using Lipofectamine 2000 reagent. [score:1]
Meanwhile, caspase-3 mRNA levels were significantly increased in the whole heart, which could be prevented by miR-98 agomir (Fig.   6F). [score:1]
We detected the functional role of miR-98 agomir in infarcted heart and found that miR-98 agomir significantly reduced the infarct size in MI (Fig.   7A and B). [score:1]
Based on the above results, we subsequently aimed to evaluate the effects of miR-98 overexpression on cell apoptosis. [score:1]
Before coronary artery ligation, miR-98 agomir was administered, which caused a continuous elevation of miR-98 (Fig.   1D). [score:1]
n = 6. (C) Upper panels show representative fluorescent images of JC-1 monomeric mitochondria showing green fluorescence and JC-1 aggregated mitochondria from Control, H [2]O [2], H [2]O [2] + NC and H [2]O [2] + miR-98 mimic groups. [score:1]
We validated the miR-98 level using Real-time PCR, and found that miR-98 level was significantly higher in miR-98 mimic transfection group than that in non-transfection group (Fig.   1C). [score:1]
However, the role of miR-98 in MI -induced cardiomyocyte apoptosis remains unknown. [score:1]
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[+] score: 182
CTR1 expression was downregulated by hsa-mir-98-5p mimics and upregulated by hsa-mir-98-5p inhibitors (Figure 4F–4G). [score:11]
Hsa-mir-98- 5p inhibits tumor cell growth and metastasis in oral squamous cell carcinoma by targeting IGFIR [22], and its overexpression prevents glioma cell line invasion by downregulating IKKε [23]. [score:10]
Our previous study indicated that EGCG suppresses hsa-mir-98-5p expression by upregulating p53, and thus cDDP efficacy is enhanced in NSCLC cells [29]. [score:8]
Hsa-mir-98-5p reportedly inhibits tumor suppressor FUS1 expression in lung cancer [28]. [score:7]
NEAT1 inhibited hsa-mir-98- 5p expression and increased CTR1 expression in A549/cDDP cells (Figure 5H–5J). [score:7]
The results showed that EGCG stimulated CTR1 expression, indicating that NEAT1 upregulated EGCG -induced CTR1 by sponging hsa-mir-98-5p in vivo (Figure 6H). [score:6]
NEAT1 knockdown increased hsa-mir-98- 5p expression (Figure 4J) and decreased CTR1 expression (Figure 4K–4L). [score:6]
Hsa-mir-98-5p inhibition significantly increased intracellular Pt and DNA-Pt adduct accumulation in A549 cells, while NEAT1 knockdown suppressed Pt and DNA-Pt adduct absorption (Figure 4M–4N). [score:6]
EGCG treatment upregulated NEAT1 and downregulated hsa-mir-98-5p compared to the control. [score:6]
Hsa-mir-98-5p inhibitors increased CTR1 expression (Figure 5G). [score:5]
In agreement with our previous study, when A549 cells were treated with EGCG for 24 h, hsa-mir-98-5p expression was inhibited (Figure 4B). [score:5]
CTR1 and NEAT1 expression were elevated in A549/cDDP cells treated with EGCG (Figure 5D, 5F), whereas hsa-mir-98-5p expression was decreased (Figure 5E). [score:5]
Using the TargetScan, Starbase, miRanda and miRDB databases, we predicted CTR1 as a putative hsa-mir-98-5p target (Figure 4A). [score:5]
We hypothesized that NEAT1 and hsa-mir-98-5p could positively and negatively regulate EGCG -induced CTR1 gene expression, respectively. [score:4]
In NSCLC, hsa-mir-98-5p can bind ITGB3 to suppress cancer proliferation, migration and invasion [26], and in breast cancer, up- regulation of the miRNA can serve as a biomarker [27]. [score:4]
To determine whether or not hsa-mir-98-5p directly targeted the CTR1 mRNA 3′UTR, A549 cells were transfected with wild-type or mutated CTR1 3′UTR and dual luciferase activity was analyzed (Figure 4H). [score:4]
The results indicated that CTR1 was a direct target of hsa-mir-98-5p. [score:4]
Hsa-mir-98-5p and NEAT1 appear to negatively and positively regulate CTR1 gene expression, respectively. [score:4]
Hsa-mir-98-5p inhibitors enhanced cDDP and DNA-Pt adduct absorption whereas NEAT1 knockdown decreased absorption (Figure 5K–5L). [score:4]
Our previous findings indicated that EGCG enhanced cDDP efficacy by inhibiting hsa-mir-98-5p in A549 cells [29], and we speculated that CTR1 could be regulated by microRNAs. [score:4]
Transfection with the wild-type 3′UTR and hsa-mir-98- 5p inhibitors elevated luciferase activity, while the mimics reduced luciferase activity. [score:3]
To assess the relationship between hsa-mir-98- 5p, NEAT1 and CTR1, hsa-mir-98-5p mimics and inhibitors were transfected into A549 cells (Figure 4E). [score:3]
Relative NEAT1, hsa-mir-98-5p and CTR1 mRNA levels in tumor tissues were expressed as 2 [−ΔCt]. [score:3]
Dual luciferase assays were performed to validate CTR1 is a direct target of hsa-mir-98-5p. [score:3]
Our bioinformatics analysis suggested that CTR1 is a putative target of hsa-mir-98-5p. [score:3]
Further studies are needed to elucidate the NEAT1/hsa-mir-98-5p/CTR1 regulation network and determine whether NEAT1 mediates CTR1 directly. [score:3]
Hsa-mir-98-5p can also restrain stem cell proliferation in ovarian cancer [24] and inhibit prostate cancer growth [25]. [score:3]
Our study identified two non-coding RNAs, hsa-mir-98- 5p and NEAT1, which modulated CTR1 expression. [score:3]
Figure 4(A) Binding between hsa-mir-98-5p and CTR1 was predicted via the TargetScan, Starbase, miRanda and miRDB databases. [score:3]
1 × 10 [5] A549 cells were seeded into 24-well plates for 24 h. Hsa-mir-98-5p mimics or inhibitors (RiboBio, Guangzhou, China) were cotransfected with 10 μg pLUC-wt-CTR1 or pLUC-mut-CTR1 using Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA). [score:3]
Hsa-mir-98-5p mimics, inhibitors and their parental negative control was transfected into NSCLC A549, H460, H1299 cells and cDDP-resistant A549 cells. [score:3]
These results showed that the hsa-mir-98-5p/NEAT1 axis regulated CTR1 in cDDP-sensitive NSCLC cells. [score:2]
These results showed that NEAT1/hsa-mir-98-5p regulated EGCG -induced CTR1 in cDDP resistant cells. [score:2]
cn/) were performed to identify specific lncRNAs regulated by hsa-mir-98-5p. [score:2]
To our knowledge, this is the first report to show that EGCG -induced CTR1 is regulated by hsa-mir-98-5p and NEAT1 in NSCLC cells (Figure 7). [score:2]
cDDP-resistant A549 cells were employed to assess whether or not EGCG could enhance cDDP sensitivity and whether NEAT1/hsa-mir-98-5p was involved in CTR1 regulation under conditions of cDDP insensitivity. [score:2]
A schematic diagram of NEAT1/hsa-mir-98-5p/CTR1 axis regulated by EGCG in NSCLC cells. [score:2]
The hsa-mir-98-5p/NEAT1 axis regulated CTR1 in A549 cells. [score:2]
Figure 7 A schematic diagram of NEAT1/hsa-mir-98-5p/CTR1 axis regulated by EGCG in NSCLC cells. [score:2]
The hsa-mir-98-5p/NEAT1 axis regulates CTR1 in cDDP-sensitive NSCLC cells. [score:2]
Hsa-mir-98-5p belongs to the let-7 family of microRNAs (miRNAs) [15– 17] and is dysregulated in cancers of the lung [18], breast [19] and colon [20], and in esophageal squamous tumors [21]. [score:2]
We hypothesized that NEAT1 and hsa-mir-98-5p were the potential positive and negative regulators of CTR1, respectively. [score:2]
Bioinformatics analysis, including LncRNAdb and StarBase were used to explore whether lncRNAs are involved in regulating hsa-mir-98-5p. [score:2]
EGCG sensitized A549/cDDP (cDDP resistant) cells to cDDP via the NEAT1/hsa-mir-98-5p/CTR1 axis. [score:1]
suggested that hsa-mir-98-5p has complementary binding with NEAT1. [score:1]
The wild-type (wt) and mutant (mut) hsa-mir-98-5p binding site in the 3′-UTR of CTR1 were synthesized and subcloned into the pGL3 Basic vector (Promega). [score:1]
We explored the interaction between hsa-mir-98-5p, NEAT1 and CTR1 in vitro and in vivo. [score:1]
EGCG sensitized cDDP-resistant A549/cDDP cells to cDDP through NEAT1/hsa-mir-98-5p/CTR1. [score:1]
Our study showed that NEAT1 could function as a competing endogenous lncRNA in lung cancer, mediating CTR1 by sponging hsa-mir-98-5p. [score:1]
NEAT1 was predicted to have complementary binding sites with hsa-mir-98-5p (Figure 4C). [score:1]
This is the first reporting of a possible mechanism for EGCG -mediated CTR1 induction via NEAT1/hsa-mir-98-5p crosstalk in NSCLC. [score:1]
NEAT1, hsa-mir-98-5p and CTR1 mRNA extracted from tumor tissues was quantified by real-time PCR (Figure 6H). [score:1]
EGCG induced CTR1 and enhanced NSCLC cell sensitivity to cDDP via hsa-mir-98-5p and NEAT1. [score:1]
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Other miRNAs from this paper: mmu-mir-92a-2, mmu-mir-92a-1
Recent reports indicate that miR-98 can suppress the IL-10 expression in B cells; such as Exposure B10 cells to IL-13 in the culture or over expression of miR-98 reduced the expression of IL-10 in B cells [14]; miR-98 inhibits IL-10 production and endotoxin tolerance in macrophages [15]. [score:11]
Exposure to cortisol in the culture markedly increased the expression of miR-98 in B cells and the cortisol -suppressed IL-10 expression in B cells could be blocked by knocking down the miR-98 gene as we observed in the present study. [score:8]
Published data indicate that miR-98 can bind to the 3′-untranslated regions of IL-10 and thereby result in IL-10 gene repression by inhibiting translation and destabilizing transcripts [15, 25]. [score:7]
Exposure to cortisol in the culture increased the expression of miR-98 in B cells, which inhibited the expression of IL-10 in B cells. [score:7]
Based on the above information, we hypothesize that the surgery -induced psychological stress increases cortisol release, which increases miR-98 expression in peripheral B cells to inhibit the development of B10 cells of patients after heart transplantation. [score:6]
Since miR-98 can bind the 5′-UTR area of the il10 gene to repress the expression of IL-10 [15], we inferred that miR-98 might be increased in peripheral B cells and associated with the decrease in IL-10 expression. [score:5]
The mice were also received intraperitoneal injection with anti-miR-98 liposomes (or control liposomes; or anti-miR-92a liposomes) (Figure 5A), or adoptive transfer with B10 cells (or naïve B cells) (Figure 5B), or 33851 (An 11β-HSD1 inhibitor used as a cortisol inhibitor, or BSA) (Figure 5C). [score:5]
Assessment of the effects of miR-98 on suppression of IL-10 expression in B cells. [score:5]
Inhibition of miR-98, or administration of cortisol inhibitor, or adoptive transfer with B10 cells, significantly improved the allograft heart survival, suggesting that these approaches have the potential to be used in clinical heart transplantation. [score:5]
The results implicate that cortisol might up regulate the expression of miR-98 in B cells. [score:4]
MiR-98 mediates cortisol -suppressed IL-10 expression in B cells. [score:4]
The results showed that the knockdown of miR-98 reduced about 10 folds of the effects of cortisol on suppression of IL-10 in B cells. [score:4]
in mice with anti-miR-98, or cortisol inhibitor, or adoptive transfer with B10 cells. [score:3]
Assessment of effects of cortisol on expression of miR-98 in B cells. [score:3]
The expression of miR-98 in B cells was assessed by RT-qPCR. [score:3]
The fact suggests that miR-98 may mediate the effects of cortisol on suppression of IL-10 in B cells. [score:3]
Expression of miR-98 in peripheral B cells is positively correlated with urinary cortisol. [score:3]
Assessment of effects of miR-98 on expression of IL-10 in B cells. [score:3]
The results showed that cortisol did increase the expression of miR-98 in B cells in a cortisol concentration -dependent manner (Figure 3C). [score:3]
The present study has made a further step in this area by employing three approaches, including anti-miR-98, cortisol inhibitor and adoptive transfer with B10 cells, in mouse heart transplantation. [score:3]
Data reported above suggest that anti-miR-98, or cortisol inhibitor, or adoptive transfer with B10 cells might enhance the allograft heart survival. [score:3]
Therapies of anti-miR-98, or cortisol inhibitor, or adoptive transfer with B10 cells enhance the allograft heart survival in mice. [score:3]
The results showed a positive correlation (r = 0.9598, p < 0.0001) between the expression of miR-98 in peripheral B cells and the cortisol levels (Figure 3B). [score:3]
The transduction resulted about 10 folds down of the miR-98 expression in the B cells. [score:3]
MiR-98-sufficient or miR-98 -deficient B cells were incubated in the presence of LPS (lipopolysaccharide; Sigma Aldrich; 1 μg/ml) with or without the presence of cortisol for 3 days. [score:1]
To test this, we analyzed the levels of miR-98 in peripheral B cells of patients. [score:1]
Following published procedures [31], anti-miR-98 or anti-miR-92a oligonucleotides (0.086 μmol; Enke Biotech, Shenzhen, China) were mixed with a lipid mixture (Sigma Aldrich) in 200 μL of 100% ethanol and 300 μl of 20 mM citrate buffer (pH 4) at 60°C. [score:1]
Preparation of miR-98- or miR-92a -deficient B cells. [score:1]
Briefly, cells were transduced with miR-98-shRNA or miR-92a-shRNA or control shRNA lentivector-containing media (2.0 × 10 [6] viral particles/ml). [score:1]
Whether miR-98 inhibits B10 cells in patients after heart transplantation has not been investigated. [score:1]
One day prior to surgery, mice were treated with one of the following procedures: (A) Intraperitoneal injection with anti-miR-98 liposome (0.1 mg/mouse; or control liposomes; or anti-miR-92a liposomes. [score:1]
B cells were transduced with miR-98 shRNA or miR-92a shRNA carried by lentivector or control lentivector (Enke Biotech, Shenzhen, China) following the manufacturer's instructions. [score:1]
The samples were passed through the column to remove ethanol and nonencapsulated anti-miR-98. [score:1]
Preparation of anti-miR-98 liposomes. [score:1]
To corroborate the results, we prepared the miR -deficient B cells by transducing B cells with miR-98 shRNA-laden lentivirus or control lentivirus. [score:1]
Administration with anti-miR-98 liposomes significantly extended the allograft heart survival in mice. [score:1]
Our data also show that higher levels of miR-98 were detected in the peripheral B cells of patients after heart transplantation, which is positively correlated with the serum cortisol levels and negatively correlated with the IL-10 mRNA levels in B cells. [score:1]
The results showed that mice received saline, or control reagent/cells, lived less than 10 days, while those treated with anti-miR-98 liposomes, or 33851, or B10 cells, lived more than 30 days (Figure 5). [score:1]
Assessment of miR-98 in B cells. [score:1]
Anti-miR-98 (anti-miR-92a, or control miR): Mice were also anti-miR-98 liposomes (or anti-miR-92a liposomes, or control liposomes). [score:1]
The miR-98 -deficient and wild B cells were exposed to LPS or/and cortisol in the culture for 48 h. The B cells were analyzed by RT-qPCR. [score:1]
The bars indicate the miR-98 levels in peripheral B cells of healthy subjects and patients. [score:1]
Assessment of miR-98 and IL-10 mRNA in B cells by real time RT-PCR (RT-qPCR). [score:1]
The results showed that the levels of miR-98 were increased in B cells after heart transplantation (Figure 3A). [score:1]
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6
[+] score: 124
First, miR-98 upregulated caspase-3 expression indirectly by down regulating the expression of upstream inhibitors that would otherwise inhibit caspase-3 expression. [score:16]
Thus, the present results provide evidence that miR-98 accelerated oocyte aging by promoting intracellular Ca [2+] release via upregulating caspase-3. Our result that miR-98 upregulated caspase-3 expression is in conflict with the general rule that miRNAs function by causing mRNA translational inhibition or degradation [20, 21]. [score:13]
However, other studies found that miR-98 suppressed apoptosis by down regulating Fas expression [70] or by directly targeting caspase-3 [71, 72]. [score:9]
Second, miR-98 directly upregulated caspase-3 expression. [score:7]
The mimics, inhibitors and control injected included mmu-miR-98 mimics (miR10000545-1-2, Guangzhou RiboBio), miRNA mimic control (miR01101-1-2, Guangzhou RiboBio), mmu-miR-98 inhibitors (miR20000545-1-2, Guangzhou RiboBio) and miRNA inhibitor control (miR02101-1-2, Guangzhou RiboBio). [score:7]
MicroRNA-98 impaired oocyte calcium stores while up regulating caspase-3. Caspase-3 expression in oocytes microinjected with miR-98 mimic or inhibitor. [score:6]
There are two possible mechanisms for miR-98 to upregulate caspase-3 expression. [score:6]
Target Scan Mouse (Release 6.2) analysis predicted that miR-98 might regulate caspase-3 expression. [score:6]
The current results show that miR-98 upregulated the expression of caspase-3, which enhanced the Ca [2+] release from the endoplasmic reticulum, leading to increased STAS. [score:6]
Figure 6 Freshly ovulated oocytes recovered at 13 h post hCG were injected with miR-98 mimic (MM) or miRNA mimic negative control (MC), or with miR-98 inhibitor (IN) or inhibitor negative control (IC), before aging culture in CZB medium. [score:5]
Figure 5Freshly ovulated oocytes recovered at 13 h post hCG were injected with miR-98 mimic (MM) or miRNA mimic negative control (MC), or with miR-98 inhibitor (IN) or inhibitor negative control (IC), before aging culture in CZB medium. [score:5]
Freshly ovulated oocytes recovered at 13 h post hCG were injected with miR-98 mimic (MM) or miRNA mimic negative control (MC), or with miR-98 inhibitor (IN) or inhibitor negative control (IC), before aging culture in CZB medium. [score:5]
In other words, up- and down -regulating miR-98 expression promoted and alleviated oocyte aging, respectively. [score:4]
At 36 h or 30 h of aging culture, caspase-3 expression was higher in oocytes injected with miR-98 mimics but was lower significantly in oocytes injected with inhibitors, compared with that in control oocytes injected with MC or IC (Fig. 6). [score:4]
The results suggest that miR-98 accelerated calcium release into cytoplasm by up regulating caspase-3 expression. [score:4]
We thus hypothesized that miR-98 might facilitate calcium release by up regulating caspase-3 expression. [score:4]
The effect of miR-98 on caspase-3 expression was thus observed. [score:3]
Mimics or inhibitors of miR-98 were microinjected into 13-h oocytes before aging culture. [score:3]
Activation rates and calcium stores in oocytes microinjected with miR-98 mimic (upper row) or inhibitor (lower row). [score:3]
In addition, this study shows that miR-98 facilitated oocyte aging by increasing Ca [2+] release through activating caspase-3. There are also reports that miR-98 promoted apoptosis by down regulating Bcl-xl [42], HMGA2 [41] or cyclin D2 [69]. [score:2]
The concentration of Taqman probe was 200 nM for U6, mmu-miR-15a, mmu-miR-16, mmu-miR-21, mmu-miR-29b and mmu-miR-128, and 400 nM for mmu-miR-98. [score:1]
Among them, whereas miR-21, miR-98 and miR-128 showed a fold change greater than 2 (FC>2), miR-15a, miR-16 and miR-29b had a fold change less than 2 (FC<2). [score:1]
The results suggest that miR-98 increased oocyte STAS by facilitating calcium leak from the endoplasmic reticulum into the cytoplasm. [score:1]
Among the 6 apoptosis-related miRNAs we selected for, whereas miR-21 was antiapoptotic [33, 34], miR-29b [35, 36], miR-15a and miR-16 [37, 38], miR-128 [39, 40] and miR-98 [41, 42; the present results] were pro-apoptotic. [score:1]
Because parthenogenetic activation of mammalian oocytes is associated with cytoplasmic Ca [2+] increases [27, 28], we observed effects of miR-98 on calcium stores of aging oocytes. [score:1]
By 36 h or 30 h of culture, however, while the calcium store in oocytes injected with miR-98 MM was lower, that in oocytes injected with IN was higher significantly than that in respective control oocytes. [score:1]
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[+] score: 101
Overexpression of miR-98 inhibited LPS -induced IL-10 expression [8]. [score:7]
Administration with Gal1 suppressed the expression of miR-98 in CD14+ cells and inhibited the OIAS in mice. [score:7]
The present data demonstrate that miR-98 expression was enhanced in CD14+ cells of OIAS mice and negatively correlated with the expression of IL-10. [score:5]
The results showed a negative correlation between miR-98 and IL-10 expression in CD14+ cells (Figure 3D), suggesting miR-98 might interfere with the expression of IL-10. [score:5]
A recent report indicated that miR-98 suppressed the expression of IL-10 in macrophages. [score:5]
The authors found that miR-98 targeted the 3′untranslated region of the IL-10 transcript. [score:5]
Published data indicate that miR-98 suppresses the expression of IL-10 [8]. [score:5]
Gal1 suppresses miR-98 and reverses IL-10 expression in CD14+ cells. [score:5]
We then tested the role of Gal1 in the regulation of miR-98 expression in CD14+ cells. [score:4]
Since CD45 is the receptor of Gal1 [12], we next assessed if CD45 mediates the effects of Gal1 in the regulation of the expression of IL-10 and miR-98 in CD14+ cells. [score:4]
CD14+ cells from the intestinal mucosa of OIAS mice showed lower levels of IL-10 expression and higher levels of miR-98; the latter could be up regulated by exposure to IL-4 in the culture. [score:4]
The results showed that the CD45 -deficient CD14+ cells did not respond the stimuli of Gal1 (Figure 4C–4D), indicating that Gal1 modulates the expression of miR-98 and IL-10 in CD14+ cells via ligating CD45. [score:3]
IL-4 increases miR-98 expression in CD14+ cells. [score:3]
Gal1 suppresses miR-98 in CD14+ cells. [score:3]
To test this, we isolated CD14+ cells from naive mouse intestine and stimulated with IL-4 in the culture for 48 h. The results showed that IL-4 did enhance the expression of miR-98 in CD14+ cells in an IL-4 concentration -dependent manner (Figure 4B). [score:3]
CD14+ cells from allergic mice express higher levels of miR-98 and lower levels of IL-10. [score:3]
Since the frequency of IL-10+ B cells was lower in CD14+ cells of allergic mice as shown by Figure 2, we inferred that the expression of miR-98 might be higher in the CD14+ cells of allergic mice. [score:3]
Treating mice with both Gal1 and PE, or Gal1 alone did not increase the expression of miR-98 in CD14+ cells (Figure 3A). [score:3]
The cells expressed high levels of miR-98. [score:3]
CD45 mediates the effects of Gal1 on modulating the expression of IL-10 and miR-98 in CD14+ cells. [score:3]
The allergy mouse-derived CD14+ cells were treated with Gal1 in the culture for 48 h. Indeed, Gal1 inhibited the levels of miR-98 in CD14+ cells (Figure 4C). [score:3]
The data implicate that IL-4 may enhance the expression of miR-98 in CD14+ cells. [score:3]
The levels of miR-98 A. IL-10 mRNA B. and IL-10 protein C. in CD14+ cells; the cells were isolated from LPMCs of mice treated with the reagents denoted on the X axis. [score:1]
C. the levels of miR-98 in CD14+ cells isolated from the OIAS mouse intestine after exposure to Gal1 in the culture for 48 h. D. the levels of IL-10 mRNA in CD14+ cells isolated from the allergic mouse intestine after exposure to Gal1 and LPS in the culture for 48 h. E. the CD45 RNAi results; (a) CD14+ cells were treated with CD45 RNAi; (b) CD14+ cells were treated with control RNAi. [score:1]
We then performed a correlation test with the data of serum IL-4 and the miR-98 levels in CD14+ cells isolated from LPMCs of allergic mice; the results showed a positive correlation (Figure 4A). [score:1]
A correlation test was performed with the data of miR-98 and IL-10 mRNA in CD14+ cells. [score:1]
B. the levels of miR-98 in CD14+ cells. [score:1]
The results showed that the levels of miR-98 were detectable in CD14+ cells of naive control mice, which was significantly enhanced in allergic mice. [score:1]
A. positive correlation between serum IL-4 levels and miR-98 in intestinal CD14+ cells of allergic mice. [score:1]
D., the negative correlation between IL-10 mRNA and miR-98 in CD14+ cells of the allergic mouse intestine. [score:1]
The levels of IL-10 mRNA and miR-98 were assessed by RT-qPCR. [score:1]
miR-98 and IL-10 levels in CD14+ cells. [score:1]
Figure 4 A. positive correlation between serum IL-4 levels and miR-98 in intestinal CD14+ cells of allergic mice. [score:1]
Figure 3The levels of miR-98 A. IL-10 mRNA B. and IL-10 protein C. in CD14+ cells; the cells were isolated from LPMCs of mice treated with the reagents denoted on the X axis. [score:1]
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8
[+] score: 69
Putative targets of nine differentially expressed miRNAs that were validated by RT-qPCR (upregulated: mmu-miR-151-3p, mmu-miR-155-5p, mmu-miR-181a-5p, and mmu-miR-328-3p; and downregulated: mmu-miR-21a-5p, mmu-miR-98-5p, mmu-miR-145a-5p, mmu-miR-146b-5p, and mmu-miR-374b-5p) were obtained from the miRWalk database. [score:11]
MyD88 Plays an Important Role in Regulating the Expression of miRNAs During B. abortus InfectionSince innate immunity is the first line of host immune defense against bacterial pathogens and our group has previously demonstrated the important role of MyD88 adaptor molecule during B. abortus infection (25), we evaluated the influence of MyD88 during differential expression of miRNAs upregulated (mmu-miR-181a-5p and mmu-miR-328-3p) or downregulated (mmu-miR-21a-5p, mmu-miR-98-5p, and mmu-miR-146b-5p) by infection. [score:10]
Differential expression of validated upregulated miRNAs (A) mmu-miR-181a-5p and (B) mmu-miR-328-3p or validated downregulated miRNAs (C) mmu-miR-21a-5p, (D) mmu-miR-98-5p, and (E) mmu-miR-146b-5p were assessed by real-time PCR and normalized to SNORD61 in bone marrow-derived macrophages from C57BL/6 and MyD88 KO mice. [score:9]
According to the expression levels and fold-change comparing Brucella-infected versus NI libraries, we selected four miRNAs that were upregulated (mmu-miR-151-3p, mmu-miR-155-5p, mmu-miR-181a-5p, and mmu-miR-328-3p) and five miRNAs that were downregulated (mmu-miR-21a-5p, mmu-miR-98-5p, mmu-miR-145a-5p, mmu-miR-146b-5p, and mmu-miR-374b-5p) for validation and further analysis. [score:9]
Validated upregulated miRNAs (F) mmu-miR-181a-5p and (G) mmu-miR-328-3p or validated downregulated miRNAs (H) mmu-miR-21a-5p, (I) mmu-miR-98-5p, and (J) mmu-miR-146b-5p were also assessed by real-time PCR in spleens from C57BL/6 and MyD88 KO mice. [score:7]
For further validation, we chose four upregulated (mmu-miR-151-3p, mmu-miR-155-5p, mmu-miR-181a-5p, and mmu-miR-328-3p) and five downregulated (mmu-miR-21a-5p, mmu-miR-98-5p, mmu-miR-145a-5p, mmu-miR-146b-5p, and mmu-miR-374b-5p) miRNAs (Table S6 in) in infected samples by real-time PCR in macrophages. [score:7]
Since innate immunity is the first line of host immune defense against bacterial pathogens and our group has previously demonstrated the important role of MyD88 adaptor molecule during B. abortus infection (25), we evaluated the influence of MyD88 during differential expression of miRNAs upregulated (mmu-miR-181a-5p and mmu-miR-328-3p) or downregulated (mmu-miR-21a-5p, mmu-miR-98-5p, and mmu-miR-146b-5p) by infection. [score:7]
On the other hand, we observed a dependence of MyD88 for the downregulation of mmu-miR-21a-5p, mmu-miR-98-5p, and mmu-miR-146b-5p during B. abortus infection in macrophages. [score:4]
By contrast, five miRNAs were validated as downregulated: (E) mmu-miR-21a-5p, (F) mmu-miR-98-5p, (G) mmu-miR-145a-3p, (H) mmu-miR-146b-5p, and (I) mmu-miR-374b-5p. [score:4]
C57BL/6 mice were infected intraperitoneally at 1, 3, or 6 days post-infection, and the relative expression of miRNAs: (A) mmu-miR-151-3p, (B) mmu-miR-155-5p, (C) mmu-miR-181a-5p, (D) mmu-miR-328-3p, (E) mmu-miR-21a-5p, (F) mmu-miR-98-5p, (G) mmu-miR-145a-3p, (H) mmu-miR-146b-5p, and (I) mmu-miR-374b-5p were evaluated in mouse spleens. [score:1]
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[+] score: 51
MiR-222 expression of celecoxib and aspirin are shown in A & B, while C & D are the miR-98 expression of celecoxib and aspirin, respectively. [score:5]
The mRNA expression of MYC and E2F2 was examined as a follow-up study to the differential expression of miR-98 as shown above. [score:5]
Figure 9 Protein expression in miR-98 and miR-222 over-expressed MCF-7aro cells. [score:5]
Compared to the control, androgen administration suppressed the expression of miR-222 and miR-98. [score:4]
Among these, miR-98 (Figure  5A) and miR-222 (Figure  5B) were downregulated in AD mice. [score:4]
Total mRNA was extracted from tumors and miRNA expression of miR-98 (A), 222 (B), 145 (C) was quantified by real-time PCR. [score:3]
Figure 8 MiR-98 and miR-222 expression in MCF-7aro cells treated with aspirin and celecoxib. [score:3]
The null result of miR-98 expression in cultures after aspirin treatment was inconsistent with the animal study data. [score:3]
Total mRNA was extracted from cells and miRNA expression of miR-98 and 222 was quantified by real-time PCR. [score:3]
Aspirin and celecoxib could reverse the suppression of miR-98 and miR-222, respectively. [score:3]
Ten μM celecoxib significantly (P < 0.05) reversed the suppression of miR-222 (Figure  8A), whereas no significant changes were observed for miR-98 (Figure  8C) or those cultures treated with aspirin (Figure  8B & D). [score:3]
MiR-98 may interact with and reduce the expression of CYP19 [43], c-Myc and E2F2 [28] in cells. [score:2]
Aspirin could act indirect in controlling miR-98. [score:2]
A recent study has documented that MYC and E2F2 can be regulated by miR-98 [28]. [score:2]
MCF-7aro cells were cultured in OptiMEM (Invitrogen Life Technology) and transfected with miR-222 or miR-98 mimics (Invitogen Life Technology) in Lipofectamine 2000 (Invitrogen Life Technology). [score:1]
In order to investigate the connection between miR-222/-98 and the protein expression profile, MCF-7aro cells were transfected with mimic miR-222 and miR-98. [score:1]
Cells are treated with androstenedione and transfected with miR-98 or miR-222. [score:1]
Expression of breast cancer -associated miRNAs, including miR-let-7c, miR-let-7 g, miR-98, miR-221, miR-222, miR-101, miR-145 and miR-17-5p, in the xenografts was also measured. [score:1]
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10
[+] score: 30
Indeed, an indirect up-regulation of HO-1 gene expression by miR-98 action has been related with oxidative stress injury in hepatocytes 31 and, similar to the induction of plasma miR-98 demonstrated here, HO-1 expression in liver was shown to increase in mice at the beginning of HT1 pathological process 19 32. [score:9]
The variation of miR-98, miR-200b and miR-409 plasmatic expression was validated at different time-point of HT1 disease. [score:5]
MiR-98 and miR-200b were shown to be up-regulated from the first week following HT1 onset a moment which corresponds to the previously reported drastic increase in alanine transaminase (hepatocyte inflammation) serum levels 26. [score:4]
Since combined increased expression of miR-98 and miR-200b has also been connected with differentiation stage of cancer phenotype progression 23, the high levels of these molecules in plasma of mice after NTBC removal (Fig. 3c,d), warrants further validation of these molecules as potential biomarkers of liver injury in HT1 patients. [score:3]
Among these, several miRNAs including let-7/miR-98 family, miR-21, miR-34a/c, miR-142, miR148a, and miR-192 predominantly expressed in liver, exhibited elevated changes in plasma samples 20. [score:3]
Graph represents 3 individual per time point and median levels of miR-98-5p (c), miR-200b-3p (d) and miR-409-5p (e) in healthy controls and in NTBC-withdrawn mice (i. e. 1 week off, 4 weeks off and 8 weeks off). [score:1]
Modulation of plasma levels of miR-98, miR-200b and miR-409 after NTBC withdrawal. [score:1]
Interestingly, among the 16 miRNAs having >1000 normalized reads in at least one plasma sample (Table 2), several miRNAs (e. g. let-7/miR98 family members, miR-200b, miR-21a, miR-142, miR-192, miR-148a) have already been reported for their implication in liver carcinogenesis and other pathological conditions 13 20. [score:1]
To confirm the modulation of specific miRNAs during progression of the HT1 -induced liver pathology in fah [−/−] mice after NTBC removal, three miRNAs (namely miR-200b-3p, miR-98-5p and miR-409-5p) were selected for validation by RT-qPCR (Table 2, highlighted miRNAs). [score:1]
Interestingly, miR-98-5p and miR200b-3p showed significant changes in circulating levels prior to AFP protein increase in liver, revealing a potential use as diagnostic tools (Figs. 3c,d and 4). [score:1]
Specifically miR-98-5p and miR-200b-3p changed significantly from the early stage of HT1 manifestation (Fig. 3c,d). [score:1]
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11
[+] score: 25
Through integrative miRNA/mRNA expression profiling, we found that miR-758 and miR-98-5p may regulate MAPK11 expression (Fig. 10D), and decreased expression of these two miRNAs in Sertoli cells (Fig. 10E) and testes of mice (Fig. 10F) may promote MAPK11 protein expression. [score:10]
MC-LR stimulation significantly inhibits miR-98-5p and miR-758 expression, resulting in enhanced expression of MAPK11. [score:7]
Through integrative miRNA/mRNA expression profiling, we found that miR-758 and miR-98-5p may regulate MAPK11 expression. [score:6]
miR-98-5p and miR-758 regulatory networks involved in microcystin-leucine arginine (MC-LR) -induced tumor necrosis factor-α (TNF-α) production in Sertoli cells. [score:2]
[1 to 20 of 4 sentences]
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[+] score: 22
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-19a, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-33a, hsa-mir-96, hsa-mir-98, hsa-mir-103a-2, hsa-mir-103a-1, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-30a, mmu-mir-30b, mmu-mir-99b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-146a, mmu-mir-155, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-191, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-221, hsa-mir-223, hsa-mir-200b, mmu-mir-299a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-146a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-96, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-148b, mmu-mir-351, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, mmu-mir-19a, mmu-mir-25, mmu-mir-200c, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-30c-1, hsa-mir-299, hsa-mir-99b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-375, mmu-mir-375, hsa-mir-148b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, mmu-mir-433, hsa-mir-429, mmu-mir-429, mmu-mir-365-2, hsa-mir-433, hsa-mir-490, hsa-mir-193b, hsa-mir-92b, mmu-mir-490, mmu-mir-193b, mmu-mir-92b, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-299b, mmu-mir-133c, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Figure 8The Prdm1 targeting miRNAs miR-23b, miR-125a, miR-351, miR-30a/c/d, miR-182, miR-96, miR-98, miR-200b/c, and miR-365 are upregulated by HDI. [score:6]
In addition to miR-23b, miR-30a, and miR-125b, which, as we showed by qRT-PCR and miRNA-Seq, are upregulated by HDI, several other putative Prdm1 targeting miRNAs, including miR-125a, miR-96, miR-351, miR-30c, miR-182, miR-23a, miR-200b, miR-200c, miR-365, let-7, miR-98, and miR-133, were also significantly increased by HDI. [score:6]
While let-7 miRNAs were not consistently altered by HDI, miR-98 was significantly upregulated by HDI in B cells in all the three experiments of CSR/plasma cell differentiation induction (p = 0.02). [score:4]
org), we identified miR-125a, miR-125b, miR-96, miR-351, miR-30, miR-182, miR-23a, miR-23b, miR-200b, miR-200c, miR-33a, miR-365, let-7, miR-98, miR-24, miR-9, miR-223, and miR-133 as PRDM1/Prdm1 targeting miRNAs in both the human and the mouse. [score:3]
miR-98 potentially target the same site as let-7 in Prdm1 3′ UTR. [score:3]
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13
[+] score: 20
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-21, hsa-mir-23a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-98, hsa-mir-99a, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-99a, mmu-mir-127, mmu-mir-128-1, mmu-mir-136, mmu-mir-142a, mmu-mir-145a, mmu-mir-10b, mmu-mir-182, mmu-mir-183, mmu-mir-187, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-139, hsa-mir-10b, hsa-mir-182, hsa-mir-183, hsa-mir-187, hsa-mir-210, hsa-mir-216a, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-224, hsa-mir-200b, mmu-mir-302a, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-128-1, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-127, hsa-mir-136, hsa-mir-193a, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-96, hsa-mir-200c, mmu-mir-17, mmu-mir-139, mmu-mir-200c, mmu-mir-210, mmu-mir-216a, mmu-mir-219a-1, mmu-mir-221, mmu-mir-222, mmu-mir-224, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-200a, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-363, mmu-mir-363, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-371a, hsa-mir-18b, hsa-mir-20b, hsa-mir-452, mmu-mir-452, ssc-mir-106a, ssc-mir-145, ssc-mir-216-1, ssc-mir-217-1, ssc-mir-224, ssc-mir-23a, ssc-mir-183, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-128-1, ssc-mir-136, ssc-mir-139, ssc-mir-18a, ssc-mir-21, hsa-mir-146b, hsa-mir-493, hsa-mir-495, hsa-mir-497, hsa-mir-505, mmu-mir-20b, hsa-mir-92b, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, hsa-mir-671, mmu-mir-216b, mmu-mir-671, mmu-mir-497a, mmu-mir-495, mmu-mir-146b, mmu-mir-708, mmu-mir-505, mmu-mir-18b, mmu-mir-493, mmu-mir-92b, hsa-mir-708, hsa-mir-216b, hsa-mir-935, hsa-mir-302e, hsa-mir-302f, ssc-mir-17, ssc-mir-210, ssc-mir-221, mmu-mir-1839, ssc-mir-146b, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-128-2, ssc-mir-143, ssc-mir-10b, ssc-mir-23b, ssc-mir-193a, ssc-mir-99a, ssc-mir-98, ssc-mir-92a-2, ssc-mir-92a-1, ssc-mir-92b, ssc-mir-142, ssc-mir-497, ssc-mir-195, ssc-mir-127, ssc-mir-222, ssc-mir-708, ssc-mir-935, ssc-mir-19b-2, ssc-mir-19b-1, ssc-mir-1839, ssc-mir-505, ssc-mir-363-1, hsa-mir-219b, hsa-mir-371b, ssc-let-7a-2, ssc-mir-18b, ssc-mir-187, ssc-mir-218b, ssc-mir-219a, mmu-mir-195b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-31, ssc-mir-182, ssc-mir-216-2, ssc-mir-217-2, ssc-mir-363-2, ssc-mir-452, ssc-mir-493, ssc-mir-671, mmu-let-7k, ssc-mir-7138, mmu-mir-219b, mmu-mir-216c, mmu-mir-142b, mmu-mir-497b, mmu-mir-935, ssc-mir-9843, ssc-mir-371, ssc-mir-219b, ssc-mir-96, ssc-mir-200b
Compared with pEFs, expression of ssc-miR-145-5p and ssc-miR-98 were down-regulated in both two types of piPSCs (Fig 2D), whereas ssc-miR-1839-5p and ssc-miR-31 were both up-regulated in both types of piPSCs (Fig 2E). [score:8]
MiR-98 belongs to the let-7 family and also targets MYC [38]. [score:3]
Compared with pEFs, miRNAs such as ssc-miR-145-5p and ssc-miR-98 were significantly down-regulated in both types of piPSCs. [score:3]
To validate the differential expression identified by the miRNA sequencing, ssc-miR-145-5p, ssc-miR-98, ssc-miR-31 and ssc-miR-1839-5p were selected for quantitative stem-loop RT-PCR analysis. [score:3]
adj ssc-miR-21 -1.1788 1.45E-02 1.68E-02 -2.4642 2.07E-04 3.85E-04 ssc-miR-143-3p -1.1940 1.40E-02 1.67E-02 -2.7004 2.27E-05 5.34E-05 ssc-miR-145-3p -1.2289 2.47E-02 2.68E-02 -2.6837 6.34E-04 1.10E-03 ssc-miR-505 -1.3657 2.68E-02 2.82E-02 -2.1577 4.16E-02 4.16E-02 ssc-miR-98 -1.5185 3.46E-03 5.15E-03 -2.8061 7.55E-05 1.55E-04 ssc-miR-139-3p -1.6685 2. 54E-02 2.71E-02 -2.5158 1.69E-02 1.93E-02 ssc-miR-23b -1.7157 3.70E-03 5.42E-03 -2.3687 8.39E-03 1.10E-02 ssc-miR-224 -1.8515 1.41E-02 1.67E-02 -2.5778 1.95E-02 2.19E-02 ssc-miR-23a -1.8753 3.40E-03 5.15E-03 -2.4676 1.00E-02 1.24E-02 ssc-miR-143-5p -1.9243 1.15E-04 2.60E-04 -3.9943 1.25E-09 5.88E-09 ssc-miR-139-5p -2.1198 2.01E-02 2.24E-02 -3. 2644 1.01E-02 1.24E-02 ssc-miR-222 -2.2666 2.58E-07 1.02E-06 -2.6019 2.34E-05 5.35E-05 ssc-miR-671-5p -2.3068 1.15E-02 1.47E-02 -2.7986 3.86E-02 3.92E-02 ssc-miR-9843-3p -2.3507 9.68E-04 1.87E-03 -4.7281 5.90E-05 1.31E-04 ssc-miR-145-5p -2.7059 2.08E-03 3.50E-03 -4.3459 7.18E-05 1.51E-04 ssc-miR-221-5p -2.7136 3.21E-07 1.21E-06 -1.9513 3.02E-02 3. 22E-02 ssc-miR-221-3p -2.9643 8.31E-11 5.47E-10 -2.1967 1.74E-03 2.90E-03 ssc-miR-708-5p -4.0615 2.31E-06 7.60E-06 -2.8238 6.43E-03 8.72E-03 ssc-miR-193a-3p -4.1933 2.39E-07 1.02E-06 -4.3848 2.87E-07 9.18E-07 ssc-miR-193a-5p -4.1933 2.39E-07 1.02E-06 -7.1423 2.32E-12 1.33E-11 ssc-miR-452 -4.3025 5.55E-11 3.99E-10 -2.2057 1.53E-02 1.77E-02 ssc-miR-206 -5.3001 6. 39E-09 3.37E-08 -6.2200 3.10E-09 1.38E-08 10.1371/journal. [score:1]
The present findings indicate that the fibroblast-enriched miRNAs, such as ssc-miR-145-5p and ssc-miR-98, may serve as barriers to reprogramming. [score:1]
adj ssc-miR-21 -1.1788 1.45E-02 1.68E-02 -2.4642 2.07E-04 3.85E-04 ssc-miR-143-3p -1.1940 1.40E-02 1.67E-02 -2.7004 2.27E-05 5.34E-05 ssc-miR-145-3p -1.2289 2.47E-02 2.68E-02 -2.6837 6.34E-04 1.10E-03 ssc-miR-505 -1.3657 2.68E-02 2.82E-02 -2.1577 4.16E-02 4.16E-02 ssc-miR-98 -1.5185 3.46E-03 5.15E-03 -2.8061 7.55E-05 1.55E-04 ssc-miR-139-3p -1.6685 2. 54E-02 2.71E-02 -2.5158 1.69E-02 1.93E-02 ssc-miR-23b -1.7157 3.70E-03 5.42E-03 -2.3687 8.39E-03 1.10E-02 ssc-miR-224 -1.8515 1.41E-02 1.67E-02 -2.5778 1.95E-02 2.19E-02 ssc-miR-23a -1.8753 3.40E-03 5.15E-03 -2.4676 1.00E-02 1.24E-02 ssc-miR-143-5p -1.9243 1.15E-04 2.60E-04 -3.9943 1.25E-09 5.88E-09 ssc-miR-139-5p -2.1198 2.01E-02 2.24E-02 -3. 2644 1.01E-02 1.24E-02 ssc-miR-222 -2.2666 2.58E-07 1.02E-06 -2.6019 2.34E-05 5.35E-05 ssc-miR-671-5p -2.3068 1.15E-02 1.47E-02 -2.7986 3.86E-02 3.92E-02 ssc-miR-9843-3p -2.3507 9.68E-04 1.87E-03 -4.7281 5.90E-05 1.31E-04 ssc-miR-145-5p -2.7059 2.08E-03 3.50E-03 -4.3459 7.18E-05 1.51E-04 ssc-miR-221-5p -2.7136 3.21E-07 1.21E-06 -1.9513 3.02E-02 3. 22E-02 ssc-miR-221-3p -2.9643 8.31E-11 5.47E-10 -2.1967 1.74E-03 2.90E-03 ssc-miR-708-5p -4.0615 2.31E-06 7.60E-06 -2.8238 6.43E-03 8.72E-03 ssc-miR-193a-3p -4.1933 2.39E-07 1.02E-06 -4.3848 2.87E-07 9.18E-07 ssc-miR-193a-5p -4.1933 2.39E-07 1.02E-06 -7.1423 2.32E-12 1.33E-11 ssc-miR-452 -4.3025 5.55E-11 3.99E-10 -2.2057 1.53E-02 1.77E-02 ssc-miR-206 -5.3001 6. 39E-09 3.37E-08 -6.2200 3.10E-09 1.38E-08 10.1371/journal. [score:1]
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[+] score: 20
In the ileum, IPA indicated that increases in miR-34a-5p alters NF-κB; let-7g and miR-98 regulates STAT3; miR-34a, mR-188-5p, let-7a-5p, and miR-151-5p regulate MAPK; miR-20b regulates IL-10; let-7g and miR-98 regulate IL-10, IL-13, IL-6; miR-15b regulates IL-6; whereas miR-99a and miR-100 regulate TNF (Fig 8). [score:7]
CI increases not only miR-15, miR-99, and miR-100 that target IL-6 and TNF, but also let-7g and miR-98 that target STAT3, whose activation transcribes iNOS [61– 64]. [score:5]
RI and CI increase miR-34a, which regulates MAPK and NF-κB, and let-7g and miR-98, which regulate STAT3, which, in turn, transcribes the iNOS gene. [score:3]
0184393.g010 Fig 10RI and CI increase miR-34a, which regulates MAPK and NF-κB, and let-7g and miR-98, which regulate STAT3, which, in turn, transcribes the iNOS gene. [score:3]
Increases in miR-98, let-7g, miR-15b, miR-99a, and miR-100 predict to regulate STAT3, IL-10, IL-13, IL-6, and TNF. [score:2]
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[+] score: 19
For example let-7a and miR-98 may have an indirect effect on expression of Nocth1 by regulating Akt pathway. [score:5]
miR-148b −2.6183 decrease apoptosis miR-152 −2.3341 Increase cell growth miR-17 −6.2545 Bcl2, N-myc miR-181c −3.5756 proliferation and remo deling of muscles miR-190b −2.2 Binds to Ubiquitin-specific protease 46, increase cell growth miR-192 −2.4871 Increase cell growth miR-199a-3p −1.9 Activin receptor IIA, Map3k4 miR-218-1 −2.2887 Increase cell growth miR-23b −2.1623 Increase Cell growth, proliferation miR-26a −2.4565 decrease proapoptotic signaling miR-27a −2.7 Ubiquitin-conjugating enzyme E2N miR-27b −3 Ubiquitin-conjugating enzyme E2N miR-296-3p −7.3378 Increase cell growth, decrease apoptosis miR-322 8.7 Hydroxysteroid (17-beta) dehydrogenase 7 miR-455 129.249 Up-regulated brown adipocyte differentiation miR-470 3.2 TGFB -induced factor homeobox 1 miR-715 18.25 Fucosyltransferase 1 miR-7a −6.2174 Increase cell growth, decrease apoptosis miR-93 −48.423 Map3k14 (NIK) miR-98 1.8 Tripartite motif-containing 6, insulin-like growth factor 2 mRNA binding protein 1 A) C2C12 myotubes were treated with 10ng/ml of TWEAK for 18h following isolation of total RNA enriched with small RNAs. [score:4]
miR-148b −2.6183 decrease apoptosis miR-152 −2.3341 Increase cell growth miR-17 −6.2545 Bcl2, N-myc miR-181c −3.5756 proliferation and remo deling of muscles miR-190b −2.2 Binds to Ubiquitin-specific protease 46, increase cell growth miR-192 −2.4871 Increase cell growth miR-199a-3p −1.9 Activin receptor IIA, Map3k4 miR-218-1 −2.2887 Increase cell growth miR-23b −2.1623 Increase Cell growth, proliferation miR-26a −2.4565 decrease proapoptotic signaling miR-27a −2.7 Ubiquitin-conjugating enzyme E2N miR-27b −3 Ubiquitin-conjugating enzyme E2N miR-296-3p −7.3378 Increase cell growth, decrease apoptosis miR-322 8.7 Hydroxysteroid (17-beta) dehydrogenase 7 miR-455 129.249 Up-regulated brown adipocyte differentiation miR-470 3.2 TGFB -induced factor homeobox 1 miR-715 18.25 Fucosyltransferase 1 miR-7a −6.2174 Increase cell growth, decrease apoptosis miR-93 −48.423 Map3k14 (NIK) miR-98 1.8 Tripartite motif-containing 6, insulin-like growth factor 2 mRNA binding protein 1 In order to understand the interaction between different genes, we generated common networks using Ingenuity Pathway Analysis (IPA) software. [score:4]
Moreover, TWEAK also significantly increased the expression of miR-715, miR- 146a, miR-455, miR-322, mir-98, and miR-470 in TWEAK -treated C2C12 myotubes (Figure 3B). [score:3]
TWEAK increased the expression of miR-715, miR-146a, miR-455, miR-322, mir-98, and miR-470 in C2C12 myotubes. [score:3]
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[+] score: 19
miR-150 regulates MNC migration by targeting Cxcr4 Since miR microarray analysis revealed that miR-29c, miR-98/let-7 family, miR-150, miR-195 and miR-494 expression was significantly downregulated in BM-derived MNCs, we extensively examined databases for predicted targets of these miRNAs involved in MNC mobilization. [score:11]
Since miR microarray analysis revealed that miR-29c, miR-98/let-7 family, miR-150, miR-195 and miR-494 expression was significantly downregulated in BM-derived MNCs, we extensively examined databases for predicted targets of these miRNAs involved in MNC mobilization. [score:8]
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[+] score: 18
Other miRNAs from this paper: mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-27b, mmu-mir-126a, mmu-mir-127, mmu-mir-145a, mmu-mir-181a-2, mmu-mir-182, mmu-mir-199a-1, mmu-mir-122, mmu-mir-143, mmu-mir-298, mmu-let-7d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-23a, mmu-mir-27a, mmu-mir-31, mmu-mir-181a-1, mmu-mir-199a-2, mmu-mir-181b-1, mmu-mir-379, mmu-mir-181b-2, mmu-mir-449a, mmu-mir-451a, mmu-mir-466a, mmu-mir-486a, mmu-mir-671, mmu-mir-669a-1, mmu-mir-669b, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-491, mmu-mir-700, mmu-mir-500, mmu-mir-18b, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-466d, mmu-mir-466l, mmu-mir-669k, mmu-mir-669g, mmu-mir-669d, mmu-mir-466i, mmu-mir-669j, mmu-mir-669f, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-669e, mmu-mir-669l, mmu-mir-669m-1, mmu-mir-669m-2, mmu-mir-669o, mmu-mir-669n, mmu-mir-466m, mmu-mir-669d-2, mmu-mir-466o, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-466c-2, mmu-mir-669a-6, mmu-mir-466b-4, mmu-mir-669a-7, mmu-mir-466b-5, mmu-mir-669p-1, mmu-mir-669a-8, mmu-mir-466b-6, mmu-mir-669a-9, mmu-mir-466b-7, mmu-mir-669p-2, mmu-mir-669a-10, mmu-mir-669a-11, mmu-mir-669a-12, mmu-mir-466p, mmu-mir-466n, mmu-mir-486b, mmu-mir-466b-8, mmu-mir-466q, mmu-mir-145b, mmu-let-7j, mmu-mir-451b, mmu-let-7k, mmu-mir-126b, mmu-mir-466c-3
To validate the expression of some of the miRs obtained from high-throughput miR array data, we selected 2 upregulated miRs (miR-122 and miR-181b) and 3 downregulated miRs (miR-23a, miR-98, and miR-31). [score:9]
Similarly, we observed downregulated (>1.5-fold) expression of mmu-let (mmu-let-7b, 7c and 7e), miR-18b and miR-98 in fetal thymocytes post TCDD exposure and these miRs possess highly complemantary sequence with FasL 3′-UTR (Table 2) demonstrating that these miRs may be involved in FasL expression. [score:8]
miR-23a and miR-23b possessed highly omplementary sequence with Fas 3′UTR region (Table 2) whereas, miR-18b and miR-98 showed highly complementary sequence with FasL 3′UTR region (Table 2). [score:1]
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[+] score: 18
miR-98-5p has been proven to regulate the expression of A β and might be a novel target of AD [45]. [score:6]
MiR-342-5p, miR-3058-3p, let-7f-5p, miR-1961, miR-301b-3p, miR-98-5p, miR-1251-5p, miR-215-5p, miR-881-5p, miR-135a-2-3p, and miR-33-3p may regulate the expression of insulin-like growth factor 1 (IGF1) or insulin-like growth factor 2 (IGF2), two molecules that could rescue behavior and memory deficits via lowering A β levels [28, 29]. [score:4]
Considering a probe signal of over 100 as abundance, eleven of the 28 miRNAs (miR-342-3p, miR-342-5p, miR-376c-3p, miR-301b-3p, let-7f-5p, miR-539-3p, miR-491-3p, miR-10a-5p, miR-98-5p, miR-652-5p, and miR-34a-5p) were shown to have targets that are tightly related to AD and could easily be detected. [score:3]
Several miRNAs derived from our microarray analysis targeted PTEN, such as miR-376c-3p, miR-342-3p, let-7f-5p, miR-10a-5p, miR-301b-3p, miR-98-5p, miR-1251-5p, and miR-34a-5p. [score:3]
For further analysis, we chose 11 evidently different miRNAs that were conserved between both human and mouse: miR-342-3p, miR-342-5p, miR-376c-3p, miR-301b-3p, let-7f-5p, miR-539-3p, miR-491-3p, miR-10a-5p, miR-98-5p, miR-652-5p, and miR-34a-5p. [score:1]
Although it is challenging to compare our results to the results of other studies in which different tissues and species were used, several miRNAs, including let-7f-5p, miR-342-5p, and miR-98-5p, showed a similar trend in human blood and CSF [48, 49]. [score:1]
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19
[+] score: 17
Four differentially expressed miRNAs in the lung had functions in cell differentiation, protein expression and apoptosis, including promotion of muscle differentiation (miR-206), regulation of cholangiocyte expression factor (miR-98), targeting pro-apoptotic and antiapoptotic proteins (miR-494), myeloid lineage development and promoting granulocytic differentiation, and suppression of erythrocytic differentiation (miR-223). [score:13]
Various other miRNAs, such as miR-29c and miR-98, were differentially expressed in the spleen and lungs of the infected animals respectively. [score:3]
It was found that miR-494, miR-365 and miR-451 were present in liver, miR-206, miR-468 and miR-691 in spleen, and miR-223, miR-98 and miR-206 in lung. [score:1]
[1 to 20 of 3 sentences]
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[+] score: 16
For 12 MYCN -targeting miRNAs we observed significant inverse correlation to MYCN expression or activity and thus provide evidence that they regulate MYCN in a neuroblastoma tissue context: eight let-7 family miRNAs (let-7a-5p, let-7b-5p, let-7c-5p, let-7d-5p, let-7f-5p, let-7g-5p, let-7i-5p and miR-98), three miR-29 family miRNAs (miR-29a-3p, miR-29b-3p, miR-29c-3p) and miR-34a-5p. [score:6]
For miR-29c-3p and -34a-5p, no expression data was available; miR-98-5p was not expressed in LSL- MYCN;Dbh-iCre tumors. [score:5]
The top 5 miRNAs (miR-449b-5p, miR-767-5p, miR-98-5p, let-7b-5p and let-7f-5p) not reported in literature were validated by demonstrating rescue of reporter gene downregulation upon mutation of potential binding sites (Van Peer et al., in preparation). [score:5]
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[+] score: 14
Other miRNAs from this paper: mmu-mir-128-1, mmu-mir-130b, mmu-mir-338, mmu-mir-128-2
Integrins have been shown to be downregulated by microRNAs in several studies in different types of cancer, some of which regulate ITGB3 translation, such as miR-128, which is upregulated in hypoxia [81, 82], miR-98 in hypoxia and miR-338, which inhibits migration by targeting HIF1α under low-oxygen conditions [83]. [score:14]
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[+] score: 14
Similarly, miR-195 (predicted to target BDNF), and let-7b and miR-98 (both predicted to target NGF) have been shown previously in human muscle to increase with aging [45], consistent with our analysis in VO rat muscle. [score:5]
Finally, TargetScan identified the following miRNAs that are conserved in humans as likely to influence NGF transcript levels: let-7b-5p and miR-98-5p and these miRNAs share a common seed sequence (CUACCUCA). [score:3]
Of these, only miR-98-5p exhibited an increase in Sarco mouse gastrocnemius muscle (this analysis was not possible in soleus due to limited tissue). [score:1]
Note that we also saw an increase in miR-98-5p in Sarco mouse muscle, which likely reflects a normal response to denervation. [score:1]
Both let-7b-5p and miR-98-5p were increased significantly in VO rat muscle (Fig.   5c). [score:1]
In contrast to the aforementioned studies in aging muscle, most of the miRNAs studied herein have been examined in the context of experimental denervation, including miR-206 (increases after reinnervation), miR-10a-5p (increases four- to seven-fold with denervation), miR-1 (increases up to 10-fold following denervation and remains elevated after reinnervation), miR-195 (increases up to 10-fold with denervation), miR-21 (increases with denervation), miR-221 (no consistent change), miR-222 (no consistent change), and miR-98 (increases up to 10-fold with denervation) [43, 47, 48]. [score:1]
MicroRNAs predicted to influence neurotrophins: a BDNF (miR-206-3p, miR-10a-5p, miR-1b, miR-195-5p and miR-497-5p), b NT3 (miR-21-5p, miR-222-3p and miR-221-3p), and c NGF (let-7b-5p and miR-98-5p) were quantified by qPCR analysis in YA (n = 8) vs VO (n = 10) rat vastus lateralis muscle and WT (n = 8) vs Sarco (n = 7) gastrocnemius muscle. [score:1]
Finally, for NGF, our analysis revealed an increase in both let-7b-5p and miR-98-5p in VO rat muscle. [score:1]
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[+] score: 13
Upon integration of the list of miRNAs predicted to target EZH2 and the differential GBM/NNB miRNA expression ratios, we found that miR-101, miR-98, miR-137, and miR-139 were down-regulated in GBM tissue as compared to NNB and have the potential to regulate EZH2 (Supplemental Table S1B). [score:8]
Besides miR-101, we also found the predicted EZH2 targeting miRNAs miR-98, miR-137, and miR-139 to be down-regulated in GBM cells as compared to NNB tissue. [score:5]
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[+] score: 13
qRT-PCR was performed to assess the expression of endogenous let-7i-5p, miR-98-5p, miR-182a-5p and miR-183a-5p in DU145 shKHSRP-KHSRP-WT and shKHSRP-KHSRP-K87R stable cell lines Since SUMOylation regulates the translocation of many proteins between nucleus and cytoplasm [25, 43, 44], we questioned whether SUMOylation of KHSRP regulates its subcellular localization. [score:5]
As expectedly, 51 miRNAs including let-7i, let-7g, let-7e and miR-98 were up-regulated by the mutant KHSRP-K87R compared with by KHSRP-WT (Fig. 4c- d; Additional file  10: Table S4). [score:3]
All of pri-let-7e, pri-let-7g, pri-let-7i, pri-miR-98 and pri-miR-182 harbored G-rich stretches in their terminal loops, as like pri-let-7a-1 and pri-let-7a-3. b KHSRPΔN fusing with SUMO1 decreases its interaction with pri-let-7a-1 and the mature let-7a production. [score:1]
To validate the sequencing results, some miRNAs including let-7i-5p, miR-98-5p, miR-182-5p and miR-183-5p were chosen for validation by using the quantitative RT-PCR. [score:1]
In particular, of 151 KHSRP -dependent miRNAs, there were 51 miRNAs (including let-7 family let-7i, let-7e, let-7g and miR-98 etc. ) [score:1]
Moreover, by using the RNAstructure software, we analyzed the secondary structures to show short G-rich stretches in the terminal loop of these pri-miRNAs (Additional file  10: Table S4), for instances, pri-let-7a-1, pri-let-7a-3, pri-let-7e, pri-let-7g, pri-let-7i, miR-98 and pri-miR-182 (Fig. 6a). [score:1]
For instances, as like pri-let-7a-1 [9, 10], the secondary structures of pri-miRNAs including pri-let-7a-3, pri-let-7g, pri-let-7i, pri-let-7e, pri-miR-98 and pri-miR-182 contained G-rich stretches (Fig.   6a). [score:1]
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[+] score: 13
Harekrushna Panda T-DC Xiaoping L Nasser C Endometrial miR-181a and miR-98 expression is altered during transition from normal into cancerous state and target PGR, PGRMC1, CYP19A1, DDX3X, and TIMP3J Clin Endocrinol Metab. [score:5]
However, treatment with siADAM8-1 led to reduced levels of only eight miRNAs (miR-181a-2, miR-29c, miR-29c*, miR-98, miR-520c-3p, miR-93, miR-130b, and miR-720), whereas three miRNAs showed increased expression, including miR-30d, miR-20a and miR-106*b (Fig.   1d), suggesting these miRNAs may not be regulated specifically by ADAM8 or may have differential regulation via splice variants. [score:5]
Deng ZQ Yin JY Tang Q Liu FQ Qian J Lin J Over -expression of miR-98 in FFPE tissues might serve as a valuable source for biomarker discovery in breast cancer patientsInt J Clin Exp Pathol. [score:3]
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[+] score: 13
Mature ID Fold Regulation miR-135b −2.6965 miR-363 −2.5995 miR-98 −2.543 miR-132 −2.355 miR-103 −2.1776 miR-99b −2.044 miR-135a −1.8734 let-7d −1.7861 miR-130a −1.6538 miR-152 −1.6246 miR-129-5p −1.6232 miR-298 −1.6169 miR-185 −1.6035 miR-214 −1.5746 miR-140 −1.5688 miR-134 −1.5667 miR-18b −1.5607 miR-194 −1.5509 let-7f −1.5107 miR-149 −1.51 A. Scatterplot showing relative expression of miRNAs by macroarray. [score:4]
Mature ID Fold Regulation miR-135b −2.6965 miR-363 −2.5995 miR-98 −2.543 miR-132 −2.355 miR-103 −2.1776 miR-99b −2.044 miR-135a −1.8734 let-7d −1.7861 miR-130a −1.6538 miR-152 −1.6246 miR-129-5p −1.6232 miR-298 −1.6169 miR-185 −1.6035 miR-214 −1.5746 miR-140 −1.5688 miR-134 −1.5667 miR-18b −1.5607 miR-194 −1.5509 let-7f −1.5107 miR-149 −1.51 Because miRNAs typically regulate translation in animal cells, we compared CXCL10 and STAT1 protein levels in both control and Dicer [d/d] animals and cells. [score:4]
These experiments confirmed that the expression of highly affected miRNAs (such as miR-98) is indeed significantly reduced (80%) in Dicer [d/d] spleen cells. [score:3]
Thus, Cxcl10 and miR-210, miR135a/b, or Oas2 and miR-7d, miR-140, miR-98, let-7f, displayed opposite regulation in Dicer mutant cells, and may be involved in the same networks in vivo. [score:2]
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[+] score: 11
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
let-7, miR-98, miR-130a and miR-16 showed uniform levels of expression in 13 different tissues but were hardly detected in pancreas (Figure 3A). [score:3]
Similarly, let-7, miR-98, miR-16 and miR-130a are abundantly expressed in 13 of the 14 tissues (except in pancreas) (Figure 3A). [score:3]
Additionally, many other miRNAs, such as let-7, miR-98, miR-16, miR22, miR-26b, miR-29c, miR-30c and miR126, were also expressed abundantly in thymus (Figure 3). [score:3]
miR-98 is represented by 5 reads in our sequences (Table 2). [score:1]
The miR-98 sequence differs from that of the let-7 family by one nt at position 11 from the 5' end, thus miR-98 is also a member of the let-7 family. [score:1]
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[+] score: 11
Modulation of pulmonary miRNAs targeting p53 (miR-138 and miR-376c) and apoptosis (miR-98 and miR-350) is consistent with the notion that AMPK is involved in the p53 -mediated cell cycle arrest and apoptosis 2. Several miRNAs upregulated in the lung of metformin -treated mice, including miR-30b, miR-138, miR-239a, miR-342, and miR-574, are involved in stress response and inflammation and target NF κB or Tlr9 (Toll-like receptor). [score:8]
Furthermore, this drug modulated miRNAs that target angiogenesis (let-7f and miR-98), stem cell recruitment, and multidrug resistance (miR-30b). [score:3]
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[+] score: 10
Of the 20 miRNAs downregulated in crypts, 8 showed a >4.0 fold difference (miR-142-5p, miR-16-5p, miR-22-3p, miR-194-3p, miR-33-5p, miR-223-3p, miR-32-5p, miR-140-5p; Fig. 4a1, blue spots), whereas, of the 15 miRNAs upregulated in crypts, 2 showed a >3.0 fold difference (miR-192-5p, miR-98-5p) (Fig. 4a2, blue spots). [score:7]
Specifically, 5 miRNAs (miR-223-3p, miR-326-3p, miR-26a-5p, miR-103-3p, miR-98-5p; Fig. 4a1 Blue spots vs Fig. 4b1: Red spots) showed expression profiles along the crypt-villus axis in PepT1 KO opposite to those in WT mice. [score:3]
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[+] score: 9
To address this issue, we first screened the miRNAs whose expressions are modulated in 4T1 cells by miRNA microarray analysis using both total cellular miRNA and exosomal miRNA after treatment with 100 μM of EGCG for 24 h. In brief, a set of miRNAs including let-7, miR-16, miR-18b, miR-20a, miR-25, miR-92, miR-93, miR-221, and miR-320 were up-regulated, and dozens of miRNAs including miR-10a, miR-18a, miR-19a, miR-26b, miR-29b, miR-34b, miR-98, miR-129, miR-181d were down-regulated in both total cellular and exosomal fraction by EGCG treatment (data not shown). [score:9]
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[+] score: 9
Hierarchichal clustering of the miRNA data revealed significant upregulation of tumor promoter miRNAs (miR-17, miR-21, miR-31, miR-98 and miR-182) and significant downregulation of tumor suppressor miRNAs (Let7a, miR-143, miR-144, miR145, miR-30a and miR-200a) in the IECs of Apc [Min/+] mice (Figure 4A). [score:9]
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[+] score: 8
In NSCLC, it has been shown that p53 is a direct target of mir-150 [24], mir-453, and mir-98, which are involved in cisplatin -induced lung cancer cells death [27]. [score:4]
Zhang S. Zhang C. Li Y. Wang P. Yue Z. Xie S. mir-98 regulates cisplatin -induced A549 cell death by inhibiting TP53 pathway Biomed. [score:4]
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[+] score: 7
Seven miRNAs (let-7e, miR-98, miR-361, miR-26b, miR-125a-5p, let-7i, and let-7f) were significantly up-regulated in the brain but down-regulated in the liver after RDX exposure. [score:7]
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[+] score: 6
Downregulating miR-98 increased the chemotaxis of THP-1 macrophages and MCP-1 induced IL-6 expression in THP-1 cells [6]. [score:6]
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35
[+] score: 6
MiR-98-5p, miR-3968 and miR-201-3p expression levels were not found to be significantly altered (H, I, K). [score:3]
However, as shown in Figure 6, the expression levels of 3 of the 11 previously identified miRNAs (miR-98-5p, miR-3968 and miR-201-3p) were not found to be significantly altered in our qPCR -based validation, in contrast to our sequencing data. [score:3]
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[+] score: 5
Three of these candidate miRNAs were validated as being more highly expressed in the sperm from CORT -treated mice, namely miR-98 (t [(6.4)=]5.26, P=0.002), miR-144 (t [(3.9)]=5.93, P=0.008) and miR-190b (t [(7.4)]=2.73, P=0.028). [score:3]
An independent cohort of CORT -treated animals was generated to validate the five top miRNA candidates, miR-190b, miR-192, miR-449a, miR-98 and miR-144, using SNORD95 as a reference gene (Figure 5d). [score:1]
miR-192, miR-449a and miR-98 have predicted binding to Igf2 (Figure 5c). [score:1]
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[+] score: 5
For example, during SARS coronavirus infection process, miR-17 [∗], mir-574-5p, and miR-214, were up-regulated, and miR-98 and miR-223 were down regulated. [score:5]
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[+] score: 5
Similarly, we found an increased expression of let-7i-5p, miR-29a-3p, miR-29c-3p, miR-30a-5p, miR-98-5p, miR-138-5p, miR-139-5p, miR-140-5p, miR-146b-5p, miR-148b-3p, miR-181a-1-3p, miR-181a-5p, miR-194-5p, and miR-342-3p, all of which have been reported to be altered in different AD tissues (Cogswell et al., 2008; Hebert et al., 2008; Maes et al., 2009; Wang et al., 2011, 2012; Lau et al., 2013). [score:3]
Interestingly, miR28a-5p, miR-98-5p, and miR-148b-3p expression was significantly higher in sedentary SAMP8 compared with sedentary SAMR1 mice and this difference was further accentuated by exercise (Figures 2A–C). [score:2]
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[+] score: 5
The miRNAs (miR-203, miR-194, miR-98, let-7 g, and miR-155) predicted to have seed sites in the 3’UTR of Rictor were stably over expressed in the ERα [+] MCF-7 cell line and screened by qPCR for Rictor expression levels. [score:5]
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[+] score: 4
For example, miR-9 contributes to regulating MMP-13, miR-98 and miR-146, which are important for controlling the expression of tumor necrosis factor α (Jones et al., 2009). [score:4]
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[+] score: 4
The Cyp19a1 gene has also been confirmed to be a direct target of miR-378 [17] and miR-98 [18]. [score:4]
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[+] score: 4
For this analysis, we decided to use the eight miRNAs having more than 80 dysregulated targets (miR-23b [50], miR-223, miR-193b [51], miR-424, miR-20a [52], miR-98, miR-891a, and miR-566), see Figure 2. We left the custom degree constraint at the default of 1 for the subsequent ORA. [score:4]
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[+] score: 4
Despite the fact that the Let-7 family consists of eight members varying only by one to two nucleotides, only Let-7i, Let-7g and miR-98 were down-regulated by Aβ, whilst the others remained mostly unchanged. [score:4]
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[+] score: 3
For instance, high expression levels of miR-98-5p, miR-302e, miR-495-3p, and miR-613 are significantly correlated with the radiosensitivity of NSCLC patients [10]. [score:3]
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[+] score: 3
Specifically, we found nine differentially expressed miRNAs in females exposed to O [3] in proestrus: miR-694 (log fold change = 1.492), miR-9-5p (log fold change = 0.836), miR-712-5p (log fold change = 0.667), miR-181d-5p (log fold change = 0.597), miR-98-5p (log fold change = 0.558), miR-200c-3p (log fold change = 0.525), miR-221-3p (log fold change = 0.385), miR-126a-5p (log fold change = 0.421), and miR-106a-5p (log fold change = − 0.527) (Fig.   7). [score:3]
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[+] score: 3
For example, miR-155 [12, 27], miR-98 [13], miR-210 [28], miR-146 [29], miR-34a [30] have been reported to participate in the production of proinflammatory cytokines and in targeting key molecules of the innate immune response. [score:3]
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47
[+] score: 3
Liu and colleagues showed that miR-98 inhibits TLR4 -dependent IL-10 production in LPS-stimulated macrophages (68). [score:3]
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48
[+] score: 2
Multiple microRNA (miR-155, let-7e, miR-98) are involved in development of tolerance 21. [score:2]
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49
[+] score: 2
In lung cancer cells, EGCG could enhance the efficacy of cDDP by down -regulating hsa-miR-98-5p [32]. [score:2]
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50
[+] score: 2
The results of miRror2.0 for the input of mmu miR-98, mmu miR-124, mmu miR-153 and mmu miR-361 are shown. [score:1]
Figure 2A shows the difference in the mapping of the four selected mouse miRNAs (mmu-miR-124, mmu-miR-153, mmu-miR-361 and mmu-miR-98; only four miRNAs were selected for simplicity). [score:1]
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[+] score: 2
Lastly, cluster 4 is consisted of let-7f-2 and miR-98 (Table  2). [score:1]
For one, whereas the nematode and the fly have only one let-7 miRNA, higher animals (e. g., fishes and mammals) have diverse let-7 family members including let-7a, - 7b, - 7c, - 7d, - 7e, - 7f, - 7g, - 7h, - 7i, - 7j, - 7k (see below for a discussion of this nomenclature) and miR-98 (Table  1) (Lagos-Quintana et al., 2001; Lau et al., 2001; Chen et al., 2005; Landgraf et al., 2007). [score:1]
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[+] score: 1
Of the 74 metastamiRs identified in this study, we found an overlap of 16 metastamiRs, including Hsa-miR-148b, Hsa-miR-23a, Hsa-miR-100, Hsa-miR-93, Hsa-miR-125b, Hsa-miR-98, Hsa-miR-92a, Hsa-miR-29b, Hsa-miR-30c, Hsa-let-7a, Hsa-let-7b, Hsa-let-7c, Hsa-let-7e, Hsa-let-7f, and Hsa-let-7g, with the findings of other researchers. [score:1]
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53
[+] score: 1
Many additional miRNAs, including miR-98 and miR-631, are involved in myogenesis, as revealed by recent studies [32, 33]. [score:1]
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[+] score: 1
In addition, at the same time point three first emerged miRNAs with the three largest numbers of connecting edges were miR-26b, miR-23b, and miR-98 (Table  1B), which all have been reported as relevant miRNAs in cardiac hypertrophy 29– 31. [score:1]
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[+] score: 1
The bar charts on the right show the read counts of 2 miRNAs (miR-98 and miR-26a-5p) as examples. [score:1]
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[+] score: 1
The let-7 miRNA family is one of the first two miRNAs discovered in Caenorhabditis elegans, and the first known human miRNA, consisting of let-7a, b, c, d, e, f, i and miR-98 miRNAs (Roush and Slack, 2008). [score:1]
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[+] score: 1
Coskun M. Bjerrum J. T. Sei delin J. B. Troelsen J. T. Olsen J. Nielsen O. H. miR-20b, miR-98, miR-125b-1*, and let-7e* as new potential diagnostic biomarkers in ulcerative colitis World J. Gastroenterol. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-21, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-98, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-141, mmu-mir-194-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-203a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-200b, mmu-mir-300, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-21a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-343, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-135a-2, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-326, hsa-mir-135b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-21, rno-mir-26b, rno-mir-27b, rno-mir-27a, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-33, rno-mir-98, rno-mir-126a, rno-mir-133a, rno-mir-135a, rno-mir-141, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-203a, rno-mir-211, rno-mir-218a-2, rno-mir-218a-1, rno-mir-300, hsa-mir-429, mmu-mir-429, rno-mir-429, hsa-mir-485, hsa-mir-511, hsa-mir-532, mmu-mir-532, rno-mir-133b, mmu-mir-485, rno-mir-485, hsa-mir-33b, mmu-mir-702, mmu-mir-343, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, hsa-mir-300, mmu-mir-511, rno-mir-466b-1, rno-mir-466b-2, rno-mir-532, rno-mir-511, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466b-8, hsa-mir-3120, rno-mir-203b, rno-mir-3557, rno-mir-218b, rno-mir-3569, rno-mir-133c, rno-mir-702, rno-mir-3120, hsa-mir-203b, mmu-mir-344i, rno-mir-344i, rno-mir-6316, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-3569, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, rno-mir-466b-3, rno-mir-466b-4, mmu-mir-203b
By the same method, we found that MRAK081523 and Plxna4 had the same MREs for miR-218, miR-141, miR-98 and let-7. Plxna4 reportedly promotes tumour progression and tumour angiogenesis by enhancing VEGF and basic fibroblast growth factor signalling [44]. [score:1]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-21, hsa-mir-23a, hsa-mir-30a, hsa-mir-98, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-30a, mmu-mir-30b, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-132, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-150, mmu-mir-155, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-217, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-150, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-34a, mmu-mir-322, mmu-mir-338, hsa-mir-155, mmu-mir-17, mmu-mir-19a, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, mmu-mir-217, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-338, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, hsa-mir-18b, hsa-mir-503, mmu-mir-541, mmu-mir-503, mmu-mir-744, mmu-mir-18b, hsa-mir-541, hsa-mir-744, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
A let-7/miR-98 recognition site was predicted in the 3′-UTR region of dmp1 mRNA with broad conservation among vertebrates (Fig. S1). [score:1]
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Rom S Dykstra H Zuluaga-Ramirez V Reichenbach NL Persidsky Y miR-98 and let-7 g* protect the blood–brain barrier under neuroinflammatory conditionsJ Cereb Blood Flow Metab 2015 12. [score:1]
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In mice, 12 genes encode members of the Let-7 family, which includes nine slightly different miRNAs (Let-7a, Let-c, and Let-7f [all encoded by two genes], and Let-7b, Let-7d, Let-7e, Let-7g, Let-7i, and miR-98 [all encoded by one gene]). [score:1]
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