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15 publications mentioning hsa-mir-1236

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-1236. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 366
To investigate whether miR-1236-3p impacted MTA2 expression, we examined MTA2 protein levels in SGC-7901 cells transfected with miR-1236-3p mimics and MKN-45 cells transfected with miR-1236-3p inhibitor, the results showed that MTA2 was downregulated when miRNA was upregulated, and upregulated when miR-1236-3p was downregulated (Fig.   4b). [score:15]
And we demonstrated that miR-1236-3p inhibited EMT process in GC cells by up -regulating E-cadherin expression, and inhibited the expression levels of vimentin and N-cadherin, but down-regulated miR-1236-3p produced the opposite effects. [score:13]
The results showed that miR-1236-3p overexpression inhibited GC cell migration, and downregulation of miR-1236-3p expression had the opposite effect (Fig.   2c). [score:10]
In renal cell carcinoma, miR-1236-3p directly targeted the p21 promoter, and increased miR-1236 expression inhibited cell proliferation, and decreased CDK4/6 and cyclin D1 expression [19]. [score:10]
These experiments demonstrated that up-regulation of miR-1236-3p significantly inhibited the cell proliferation and reduced the number of migrated and invaded cells, and down-regulation of miR-1236-3p promoted cell proliferation and increased the number of migrated and invaded cells. [score:9]
In summary, our results showed that miR-1236-3p functioned as a tumor suppressor to inhibit cell invasion in GC by targeting MTA2 and inhibiting the EMT process. [score:9]
miR-1236-3p over -expression could inhibit GC cell proliferation, migration and invasion, and inhibition of miR-1236-3p expression had opposite effects. [score:9]
We also observed that miR-1236-3p upregulation resulted in morphological changes from an extended morphology to more organized cell–cell contacts in SGC-7901 cells, and miR-1236-3p downregulation had the opposite result in MKN-45 cells (Fig.   7). [score:7]
Upregulation or downregulation of miR-1236-3p had the same effects on MTA2 mRNA levels as proteins levels (Fig.   4c). [score:7]
To explore the potential mechanism of miR-1236-3p in GC, the miR-1236-3p candidate target genes were predicted with TargetScan, miRanda, and miRDB, and MTA2 was selected as a potential target gene for miR-1236-3p. [score:7]
Furthermore, we demonstrated that MTA2 was a candidate target of miR-1236-3p, and miR-1236-3p over -expression significantly inhibited the process of epithelial–mesenchymal transition. [score:7]
Thus, we demonstrated that miR-1236-3p functioned as a tumor suppressor in GC at least partly through inhibition of the EMT process and PI3K/Akt signaling pathway by targeting MTA2. [score:7]
Furthermore, we showed that miR-1236-3p could directly target at MTA2 and regulate its expression. [score:7]
To examine miR-1236-3p expression in GC cells, we measured the levels of miR-1236-3p in three GC cell lines, MKN-45, SGC-7901, and MGC-803, as well as a normal human gastric cell line, GES-1. The results indicated that the expression of miR-1236-3p was downregulated in MKN-45, SGC-7901, and MGC-803 cells compared with expression in GES-1 cells (Fig.   1a). [score:7]
Among the candidates, MTA2, a potent oncogene that is frequently upregulated in human cancers [25, 26], was predicted to be a miR-1236-3p target by all three of the algorithms and was selected for further experimental verification. [score:6]
Moreover, we detected the expression level of MTA2 protein in four miR-1236-3p downregulated GC tissues. [score:6]
Accumulating evidence predicts that miR-1236-3p may act as a tumor suppressor gene, and downregulation of miR-1236-3p has been demonstrated in some cancers. [score:6]
Through preliminary screening we found that miR-1236-3p is significantly down-regulated in GC, and may serve as a potential diagnostic biomarker and therapeutic target in GC. [score:6]
We predicted potential direct common target genes of miR-1236-3p using miRNA databases including TargetScan [22], miRanda [23], and miRDB [24]. [score:6]
To determine the level at which miR-1236-3p regulate MTA2 expression, we examined the expression of MTA2 mRNA after transfection. [score:6]
The aim of this study was to demonstrate the downregulated expression of miR-1236-3p in gastric cancer (GC) tissues and cell lines, and clarify its biological function in GC. [score:6]
In hepatocellular carcinoma, miR-1236-3p down-regulates alpha-fetoprotein (AFP), thus causing PTEN accumulation, which inhibits the PI3K/Akt pathway [17]. [score:6]
We demonstrated that miR-1236-3p and MTA2 showed an inverse expression pattern in GC and that their functional roles in the development of GC were exerted by regulating EMT and PI3K/Akt signaling. [score:5]
The inhibition of miR-1236-3p expression promoted cell proliferation, migration, invasion, cell epithelial–mesenchymal transition (EMT) processes, and the PI3K/Akt signaling pathway. [score:5]
Consistently, decreased cell migration was also observed when miR-1236-3p was upregulated in wound healing assays (Fig.   3a), suggesting that miR-1236-3p can suppress migration. [score:5]
Our study revealed that miR-1236-3p over -expression decreases the phosphorylation of AKT and inhibition of miR-1236-3p increases the phosphorylation of AKT. [score:5]
Collectively, our results revealed that miR-1236-3p suppressed the Akt signaling pathway partly through its target MTA2. [score:5]
Our results suggest that miR-1236-3p functions as a tumor suppressor in GC and could be a promising therapeutic target for GC. [score:5]
Thus, these results suggested that miR-1236-3p inhibited the cell invasion by partly suppressing the PI3K/Akt signaling pathway. [score:5]
The cancer tissues with higher expression of miR-1236-3p than their adjacent normal tissues were selected as the high group, while those with less expression of miR-1236-3p than their adjacent normal tissues were selected as the low group. [score:5]
MTA2 is a direct common target of miR-1236-3p. [score:4]
miR-1236-3p is downregulated in GC cell lines and specimens. [score:4]
Furthermore, the E-cadherin level was reduced but vimentin and N-cadherin levels was increased when miR-1236-3p was downregulated (Fig.   6). [score:4]
CCK-8 cell proliferation assay displayed that cell proliferation was inhibited in SGC-7901 cells transfected with miR-1236-3p mimics, but enhanced in MKN-45 cells transfected with miR-1236-3p inhibitor (Fig.   2b). [score:4]
In addition, we found that MTA2 mRNA and protein levels were negatively related to miR-1236-3p in GC cells, indicating that miR-1236-3p can negatively regulate MTA2 expression in GC. [score:4]
Moreover, miR-1236-3p down-regulation was also reported in bladder cancer, lung cancer, and breast cancer [20, 21], however, its biological function in GC is remains unclear. [score:4]
Furthermore, trans-well invasion assays suggested that miR-1236-3p overexpression significantly suppressed GC cell invasive capacity, as showed in Fig.   3b. [score:4]
miR-1236-3p down-regulation was observed in GC tissues specimens and cell lines. [score:4]
These results demonstrated that miR-1236-3p regulates MTA2 protein expression and mRNA decay at the post-transcriptional level. [score:4]
Moreover, miR-1236-3p down-regulation was clearly relative to advanced clinical stage. [score:4]
To evaluate the possibility that miR-1236-3p might regulate the EMT, we transfected SGC-7901 and MKN-45 cells with miR-1236-3p mimics or the inhibitor respectively, and then examined the expression of E-cadherin, vimentin and N-cadherin using western blotting. [score:4]
These data suggest that miR-1236-3p might act as a tumor suppressor in GC (Table  1). [score:3]
Taken together, these findings indicate that miR-1236-3p can inhibit GC cell migration and metastasis. [score:3]
Next, we employed a luciferase reporter system to confirm whether MTA2 was directly regulated by miR-1236-3p. [score:3]
We observed that miR-1236-3p inhibited the luciferase reporter activity of the wild-type MTA2 3′-UTR, but did not significantly change the luciferase reporter activity of the 3′-UTR with mutated binding sites (Fig.   4d). [score:3]
The results indicated that a low miR-1236-3p expression level was correlated with high TNM stage (P = 0.003), lymph node metastasis (P = 0.018), and differentiation (P = 0.015). [score:3]
In high-grade serous ovarian carcinoma, miR-1236-3p represses cell migration and invasion abilities by targeting ZEB1 [18]. [score:3]
After inhibition of miR-1236-3p, the cell morphology showed a tendency of mesenchymal cells. [score:3]
miR-1236-3p suppressed GC cell EMT. [score:3]
We also found that miR-1236-3p could suppress the PI3K/Akt signaling pathway in GC cells. [score:3]
These results suggested that miR-1236-3p could efficiently inhibit GC cell proliferation. [score:3]
Gastric cancer Metastasis miR-1236-3p MTA2 Epithelial–mesenchymal transition Tumor suppressor gene Gastric cancer (GC) is the second most frequent cause of cancer deaths in the world, and remains the type of cancer with the highest incidence in northeast Asia [1]. [score:3]
miR-1236-3p expression, which was associated with lymph node metastasis, differentiation and clinical stage, was significantly reduced in GC tissues and cell lines. [score:3]
We also analyzed the associations between the miR-1236-3p expression level and the clinicopathological parameters of GC patients. [score:3]
The miR-1236-3p mimic and the negative control were transfected into SGC-7901 cells, and the miR-1236-3p inhibitor and the negative control were transfected into MKN-45 cells. [score:3]
miR-1236-3p suppresses GC cell proliferation. [score:3]
miR-1236-3p inhibits the Akt signaling pathway in GC cells. [score:3]
miR-1236-3p expression was confirmed with qRT-PCR after transfection (Fig.   2a). [score:3]
b qRT-PCR analysis of miR-1236-3p expression in human GC tissue samples and their matched normal adjacent tissues from 83 GC patients. [score:3]
These results suggested a tumor suppressor role for miR-1236-3p in GC progression. [score:3]
Fig.  1The expression level of miR-1236-3p in gastric cancer tissues and cells lines. [score:3]
The lentivirus-hsa-miR-1236-3p mimic, the lentivirus-hsa-miR-1236-3p inhibitor, and a miRNA negative control (NC) were purchased from Genechem (Shanghai, China). [score:3]
a The expression of miR-1236-3p in SGC-7901 cells transfected with miR-1236-3p mimic or negative control (NC). [score:3]
miR-1236-3p target gene prediction. [score:3]
In this study, we found that after overexpression of miR-1236-3p, the cell morphology showed an epithelialization trend. [score:3]
The predicted interaction between miR-1236-3p and the target site in the MTA2 3′-UTR is illustrated in Fig.   4a. [score:3]
a qRT-PCR analysis of miR-1236-3p expression in three human GC cell lines and one normal cell line. [score:3]
miR-1236-3p inhibits GC cell migration and metastasis. [score:3]
We found that E-cadherin level was increased, but vimentin and N-cadherin levels was reduced when miR-1236-3p were over-expressed. [score:3]
miR-1236-3p has been reported to function as tumor suppressor microRNA in various malignancies. [score:3]
The miR-1236-3p-MTA2 axis provides insight into the mechanisms underlying tumor metastasis, and may serve as a promising therapeutic target for GC treatment. [score:3]
c Transwell migration assays of SGC-7901 cells transfected with miR-1236-3p mimic or NC, and MKN-45 cells transfected with miR-1236-3p inhibitor or NC. [score:2]
Dual luciferase assay was used to demonstrate that MTA2 was one of the candidate target genes of miR-1236-3p. [score:2]
Hence, these results suggested that miR-1236-3p and MTA2 were considered as new molecular biomarkers in predicting the aggressive biology of GC and novel therapeutic targets for GC. [score:2]
In our study, luciferase assays were performed and MTA2 was identified as a novel target of miR-1236-3p. [score:2]
The 3′-UTR of MTA2 contains two conserved binding sites for miR-1236-3p. [score:1]
RNA isolation and quantitative real-time PCR of miR-1236-3p. [score:1]
The wild-type or mutant 3′-UTR of the MTA2 mRNA was inserted into a luciferase reporter vector, and then each construct was co -transfected with miR-1236-3p mimics. [score:1]
To further explore the function of miR-1236-3p in GC, we performed a series of functional analyses. [score:1]
Our results showed that high levels of miR-1236-3p decreases the phosphorylation of AKT and low levels of miR-1236-3p increases the phosphorylation of AKT (Fig.   8). [score:1]
Mir-1236-3p, an intronic miRNA, is located in the Chr6p21.33 and embedded within the intron of the NELFE gene. [score:1]
In the present study, we verified the influence of miR-1236-3p on the protein levels of AKT and p-AKT. [score:1]
a Two predicted miR-1236-3p binding sites located in the MTA2 3′-UTR. [score:1]
Recent studies revealed that miR-1236-3p played a critical role in human cancers. [score:1]
The purpose of this study is to investigate miR-1236-3p expression in GC and cell lines. [score:1]
Hence, we speculated that miR-1236-3p might be associated with the EMT of gastric cells to GC. [score:1]
In this study, we examined the roles of miR-1236-3p in GC. [score:1]
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2
[+] score: 105
In our study, we discovered a novel role of miR-1236 in inhibiting HBV replication by direct targeting at HBV specific RNA. [score:6]
The microRNA, miR-1236, was found to target a sequence localized within the 3′UTR of HBV specific RNAs, leading to reduced viral gene expression. [score:5]
When the genomic dimer of HBV adr was cotransfected with a miR-1236 expression vector, both viral DNA synthesis (Fig. 3D) and secreted HBsAg (Fig. 3E) were significantly inhibited. [score:5]
As shown in Fig. 2A, miR-204 and miR-1236 could each inhibit HBV DNA replication, without altering the level of HBV RNA expression in the cytoplasm (Fig. 2B). [score:5]
Only the combination of seed mutant miR-1236 and the target site mutant of HBV significantly restored the inhibitory effect of miR-1236 on the reporter activity (Fig. 3B). [score:5]
In addition, miRNA-1236 contributes to HIV-1 restriction in monocytes 26, and has a regulatory role in alpha-fetoprotein (AFP) expression and HCC development in the liver 22. [score:5]
We also performed compensatory mutagenesis by introducing mutations into the seed sequences of miR-1236 and its predicted target site on HBV (Fig. 3B). [score:4]
How to cite this article: Huang, J. -Y. et al. MicroRNA miR-204 and miR-1236 inhibit hepatitis B virus replication via two different mechanisms. [score:3]
In a separate approach via bioinformatics analysis, we identified miR-1236 as a potential anti-HBV miRNA by using the Microinspector target-prediction algorithm. [score:3]
Shaded box highlights the seed sequence of hsa-miR-1236 and its target site sequences. [score:3]
However, expression of miR-1236 can be found in various tissues including liver 22. [score:3]
gr) were used to predict potential targets for miR-1236 and miR-204 on HBV genome. [score:3]
The expressions of miR-204 and miR-1236 were detected by stem-loop PCR analysis (Fig. S1). [score:3]
Target site mutants containing altered sequences at HBV 3′UTR and a miR-1236 mutant containing altered seed sequences, were engineered by using paired mutant primers (HBV mutant 3′UTR Forward: 5′-GGAGGAGTTGGGAGAGGAAATTAGGTTAAAGG-3′; Reverse: 5′-CCTTTAACCTAATTTCCTCTCCCAACTCCTCC-3′, miR-1236 mutant Forward: 5′-GCCAACATAATGCTTCTTCTCCTTGTCTCTCC-3′; Reverse: 5′-GGAGAGACAAGGAGAAGAAGCATTATGTTGGC-3′) and Site-directed Mutagenesis Kit (Stratagene, Santa Clara, CA). [score:3]
Interestingly, we found that hsa-miR-1236 was also reduced in expression in human HBV-producing cell lines (Fig. 1D). [score:3]
The methods of engineering the expression vectors of miR-204 and miR-1236 were as described previously 5 33. [score:3]
Expression of miR-204 and miR-1236 were reduced in HBV-replicating hepatocytes and HBV-transgenic mice. [score:3]
Lower panel: HuH-7 cells were cotransfected with wild type or mutant pGL3-HBV 3′ UTR (nt1521-2122) reporter and wild type or mutant miR-1236 expression vector. [score:3]
As shown in Fig. 3C, the target sites of miR-1236 appear to be evolutionarily conserved. [score:3]
MiR-1236 can directly target at HBV specific RNA of different genotypes. [score:3]
MicroRNA miR-204 and miR-1236 can each attenuate HBV replication and gene expression. [score:3]
Only miR-1236 and miR-130a 5 (data not shown), but not miR-204 and vector control, could reduce HBV protein expression. [score:3]
Using Computer-aided programs, we predicted potential target sites of miR-1236 and miR-204 clustering between nt 1521 and nt 2122 on the HBV ayw genome (Fig. 3A). [score:3]
Upper panel: Sequence alignment of wild type and mutant miR-1236 with putative target sites on wild type or mutant HBV genomes (nt 1724-1755). [score:3]
This result suggests a direct interaction between miR-1236 and HBV specific RNA. [score:2]
Recently, miR-1236 has also been shown to be induced by IL-1β and repressed by Twist1 to regulate the inflammatory lymphangiogenesis 23 and hypoxia -induced EMT 27. [score:2]
Knockdown of endogenous miR-204-5p or miR-1236 significantly resulted in increased HBV DNA replication (Fig. 2E) and protein synthesis (Fig. 2F). [score:2]
Interestingly, miR-1236 is found only in humans, pantroglodytes and pongopygmaeus, but not in rodents (GeneCards and miRBase version 21). [score:1]
Reduction in firefly luciferase activity was restored when mutant miR-1236 was matched with the mutant reporter (**p < 0.05). [score:1]
Therefore, miR-1236 has a negative effect against HBV subtypes other than ayw. [score:1]
Human genomic DNA extracted from HepG2 cells was used as a template for PCR amplification of precursor sequences of miR-204 and miR-1236. [score:1]
Only miR-1236 displayed significant reduction of luciferase activity (**p < 0.05). [score:1]
We also investigated whether miR-1236 can target HBV RNA of a different genotype, such as adr. [score:1]
We have no results on the tissue distribution of human miR-1236 at present. [score:1]
MiR-1236 is an intronic miRNA with no other family member (miRBase version 21). [score:1]
Briefly, the sequences of human miR-204 and miR-1236 were retrieved from Ensembl database and miRBase (Version 16). [score:1]
To further elucidate the mechanism, we cotransfected an HBV genomic replicon with LNA-miR-204-5p or LNA-miR-1236 into HepG2 cells (Fig. 2D). [score:1]
The successful bioinformatics approach to identifying miR-1236 allows us to anticipate that miR-3960, miR-3166, miR-4763, miR-665 and miR-663, are potential candidates for anti-HBV miRNA (Tables 1 and 2). [score:1]
To evaluate the effect of microRNA on viral replication, we cloned the precursors of miR-204 and miR-1236 in miRNA expression vectors, respectively. [score:1]
This LNA experiment confirmed the anti-HBV potential from miR-204-5p and miR-1236. [score:1]
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3
[+] score: 68
As shown in Figure 4B and C, the transfection of miR-1236 inhibitors enhanced the translation of VprBP in monocytes and significantly promoted the infection of HIV-Luc/VSV-G. Complementarily, when the chemically synthesized miR-1236 mimics were transfected into MDDCs, translation of VprBP was suppressed (Figure 4D), and infection of MDDCs by HIV-Luc/VSV-G was accordingly significantly diminished (Figure 4E). [score:9]
ular miR-1236 targets 3′-untranslated region (UTR) of VprBP mRNA for translation inhibition in monocytes. [score:9]
Cells were transfected by Lipofectamine 2000 (Invitrogen) with plasmids of pCMV-myc/pCMV-myc-VprBP, or with specific duplex siRNA of VprBP or off-target control (GenePharma, Shanghai, China), or with miR-1236 inhibitor or mimics (GenePharma). [score:5]
s were transfected by Lipofectamine 2000 (Invitrogen) with plasmids of pCMV-myc/pCMV-myc-VprBP, or with specific duplex siRNA of VprBP or off-target control (GenePharma, Shanghai, China), or with miR-1236 inhibitor or mimics (GenePharma). [score:5]
Given the important role of VprBP in promoting HIV-1 infection and the regulation of VprBP translation by miR-1236, we were interested in whether miR-1236 modulated monocyte/MDDC susceptibility to HIV-1 infection. [score:4]
These data demonstrate that miR-1236 -mediated regulation of VprBP expression modulates the differentiation -dependent susceptibility of monocytes/MDDCs to HIV-1 infection. [score:4]
To confirm the targeting of VprBP mRNA 3′-UTR by miRNA-1236, 3′-UTR fragments of VprBP mRNA that contained the conserved binding positions were cloned into pGL3cM, and mutations were introduced at the conserved binding positions of VprBP 3′-UTR to reduce Watson–Crick base pairing with miRNAs (Figure 3C). [score:4]
miR-1236 modulates HIV-1 infection by targeting VprBP. [score:3]
VprBP -targeted miR-1236 modulates differentiation -dependent susceptibility of monocytes/MDDCs to HIV-1 infection. [score:3]
Briefly, pGL3CM reporter plasmids (100 ng) were co -transfected into HEK293T cells with miR-1236 (1μl) or off target control and 10 ng pRL-TK. [score:3]
These data demonstrated that miR-1236 targets VprBP mRNA 3′-UTR for repression in monocytes. [score:3]
3′-UTR of VprBP mRNA is targeted by miR-1236. [score:3]
We found the 17–24 bases of VprBP 3′-UTR were targeted by hsa-miR-1236. [score:3]
In summary, our results demonstrate that host factor VprBP was targeted by cellular miR-1236 to modulate monocyte/MDDC differentiation -dependent susceptibility to HIV-1 infection. [score:3]
miR-1236 expression was significantly enhanced in monocytes compared with MDDCs (Figure 3B). [score:2]
Expression of miR-1236 was verified with Bulge-loop miRNA qRT-PCR Primer Sets. [score:2]
And point mutations of conserved binding sites of VprBP 3′-UTR for miR-1236 were synthesized as follow: 5′-CGGAGCCATCACTGCTTAACGA CAGTTCTTGGCAGAGAGAAGAGGGGACAA-3′ (forward), 5′-GATCTTGTCC CCTCTTCTCTCTGCCAAGAACTGTCGTTAAGCGTGATGGCTCCGAGCT-3′ (reverse). [score:2]
Binding sites of VprBP 3′ UTR for miR-1236 were synthesized as follows: 5′-CGGAGCCATCACTGCTTGGAAGAGATTCTTGGCAGAGAGAAGAGGGGACAA-3′ (forward), 5′-GATCTTGTCCCCTC TTCTCTCTGCCAAGAATCTCTTCCAAGCAGTGATGGCTCCGAGCT-3′ (reverse). [score:1]
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4
[+] score: 43
hsa-miR-1236-3p processed from a putative mirtron downregulates alpha fetoprotein, thus leading to the inhibition of the PI3K/Akt pathway in hepatoma cancer cell lines [20], and negatively regulates the vascular endothelial growth factor receptor VEGFR-3 during inflammatory lymphangiogenesis [21]. [score:7]
White vertical boxplots represent data from healthy tissues; gray from tumors Table 3 Expression of mirtronic miRNAs in colorectal, stomach, and pancreatic cancerous tissues compared to healthy tissues Cancerous tissue miRNAs of mirtron origin Non-mirtronic miRNA miR-1226-3p miR-1227-3p miR-1229-3p miR-1236-3p miR-1238-3p Colorectal − No change No change No change No change Stomach + No change No change No change No change Pancreatic No change − No change − No changeData were considered significant for p < 0.05 − reduced expression compared to the non-cancerous tissue, + increased expression Despite a considerable progress in the study of biogenesis of mirtron-derived miRNAs, the factors responsible for mirtronic intron splicing are not known. [score:4]
Whereas steady levels of hsa-miR-1226-3p were detected in pancreatic cancer and healthy pancreatic tissues, two other mirtronic miRNAs, hsa-miR-1227-3p (p = 0.028) and hsa-miR-1236-3p (p = 0.017), were significantly downregulated in this tumor type. [score:4]
Dendrogram of hierarchy clustering analysis is presented at the left Table 2 Differential expression of mirtronic miRNAs in pancreas, kidney, colon, and stomach cancer cell lines Organ Cell line miRNAs of mirtron origin Non-mirtronic miRNA miR-1226-3p miR-1227-3p miR-1229-3p miR-1236-3p miR-1238-3p Pancreas PANC-1−2.8 ± 1.8 [a] −1.7 ± 0.3 [a] −2.8 ± 0.9 [a] −1.4 ± 0.2 −1.2 ± 0.6 SU. [score:3]
In addition, a miR-1236-3p antisense oligonucleotide inhibits the glioma tumor cell growth and proliferation [22]. [score:3]
The expression levels of hsa-miR-1226-3p, hsa-miR-1227-3p, hsa-miR-1229-3p, and hsa-miR-1236-3p dramatically decreased and comprised less than 5 % of the levels observed for the WT minigenes (Table  1). [score:3]
T3 stage pancreatic tumors exhibited a decline of the hsa-miR-1227-3p and hsa-miR-1236-3p expression. [score:3]
86.86, T3M4, stomach KATOIII, colon HCT116) or the excretory system (kidney CaKi-1, 786-O) were chosen to define whether the expression of the human mirtronic miRNAs hsa-miR-1226-3p, hsa-miR-1227-3p, hsa-miR-1229-3p, and hsa-miR-1236-3p and canonical hsa-miR-1238-3p varies between the cancerous cells. [score:3]
The miRNA variability in cancer cell lines was determined by changes in abundance of two mirtronic miRNAs, hsa-miR-1229-3p and hsa-miR-1236-3p, while the expression levels of hsa-miR-1226-3p and hsa-miR-1227-3p declined in all tested cancer cell lines compared to those in HEK 293A. [score:2]
In this study, cell line-specific profiles of miRNAs processed from conventional mirtrons, hsa-miR-1226-3p, hsa-miR-1227-3p, hsa-miR-1229-3p, and hsa-miR-1236-3p, in seven various pancreatic, kidney, colorectal, and stomach cancer cell lines were identified (Table  2). [score:1]
Putative human conventional mirtron-derived hsa-miR-1227-3p, hsa-miR-1229-3p, hsa-miR-1236-3p, and hsa-miR-1238-3p [15] and 3′-tailed mirtron-derived hsa-miR-3940-5p and hsa-miR-6850-5p were identified in short 69–102 nucleotide introns, whereas hsa-miR-3064-5p and hsa-miR-6515-5p were processed from both long (1236 nt) and short (88 nt) 5′-tailed mirtrons [12]. [score:1]
In this study, we experimentally validated three novel splicing -dependent miRNAs processed from mirtrons, hsa-miR-1227-3p, hsa-miR-1229-3p, and hsa-miR-1236-3p. [score:1]
We found that biogenesis of the human hsa-miR-1227-3p, hsa-miR-1229-3p, and hsa-miR-1236-3p is splicing -dependent; therefore, these miRNAs can be assigned to the class of miRNAs processed by a non-canonical mirtron pathway. [score:1]
Previous studies demonstrated that cellular levels of hsa-miR-1226-3p and hsa-miR-1236-3p inversely correlate with cancerogenesis in breast and hepatoma cancer cells, respectively [20, 33]. [score:1]
In the present study, we experimentally proved that hsa-miR-1227-3p, hsa-miR-1229-3p, and hsa-miR-1236-3p derived from conventional mirtrons are processed by the splicing machinery. [score:1]
In this study, we examined eight putative mirtrons and provided experimental evidence that human hsa-miR-1227-3p, hsa-miR-1229-3p, and hsa-miR-1236-3p could be assigned to the class of mirtronic miRNAs. [score:1]
Introns containing validated mirtronic miRNA hsa-mir-1226-3p or predicted miRNAs hsa-mir-1227-3p, hsa-mir-1229-3p, hsa-mir-1236-3p, and hsa-mir-1238-3p processed from conventional; hsa-miR-3064-5p and hsa-miR-6515-5p from 5′-tailed; and hsa-miR-3940-5p and hsa-miR-6850-5p from 3′-tailed mirtrons are depicted as red lines. [score:1]
Ding K, Zhang P, Li J, Duan C, Shen X. Human miR-1236 antisense ribonucleic acid and application thereof. [score:1]
In contrast, hsa-miR-1229-3p and hsa-miR-1236-3p showed significant variations among cancer cell lines and have a potential to be exploited for profiling specific cancer cell types. [score:1]
These results convincingly confirmed that the biogenesis of hsa-miR-1226-3p, hsa-miR-1227-3p, hsa-miR-1229-3p, and hsa-miR-1236-3p is strictly splicing -dependent, thus the efficiency of the splicing machinery defines the quantity of these miRNAs. [score:1]
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5
[+] score: 27
Interestingly, among the 736 miRNAs analyzed in the first study, upregulation of miR-455-3p and miR-33a was associated with chemosensitivity while upregulation of miR-224, miR-1236, and miR-520d-3p was associated with chemoresistance [21]. [score:7]
Upregulation of miR-455-3p and miR-33a was found to be associated with chemosensitivity while upregulation of miR-224, miR-1236, and miR-520d-3p was associated with chemoresistance [21]. [score:7]
On the other hand, high expression of miR-224, miR-1236, and miR-520d-3p and low expression of miR-455-3p and miR-33a were found to be individually associated with unfavorable outcome and a score based on this five-miRNAs was proposed to predict the clinical outcome of DLBCL patients treated with R-CHOP regimen, independent from the IPI score [21]. [score:5]
In addition, a predictor score based on a signature of five miRNAs, among which high expression of miR-224, miR-1236, and miR-520d-3p and low expression of miR-455-3p and miR-33a were individually associated with unfavorable outcome, has been proposed to predict the clinical outcome of DLBCL patients, independent from the IPI score [21]. [score:5]
Five miRNAs were differentially expressed between both groups (miR-224, miR-1236, miR-520d-3p, miR-33a, and miR-455-3p) and were validated in an independent group of 133 patients. [score:3]
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[+] score: 18
Although miR-1236 is lowly expressed in human LECs, it may be upregulated during inflammation -induced lymphangiogenesis to control the expression of VEGF-C/VEGFR-3 signaling. [score:8]
IL-1β can induce miR-1236 and downregulate VEGFR-3 protein which is similarly reported in inflammatory lymphangiogenesis. [score:4]
In addition, LEC-specific genes are downregulated and miRNAs, including miR-9, miR-1236, and miR-K12-11, a viral ortholog of miR-155, contribute to the loss of LEC identity. [score:4]
VEGFR-3 was also shown to be regulated by a mirtron miR-1236, arising from a spliced-out intron that is processed independently of Drosha, in human LECs (89). [score:2]
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[+] score: 9
The diminished expression of another cellular cofactor called Vpr(HIV-1) -binding protein (VprBP) in monocytes compared to the MDDCs has also been attributed to the direct targeting of VprBP 3′UTR by the cellular miRNA miR-1236 [231]. [score:5]
Knockdown of miR-1236 in monocytes or overexpression in MDDCs increased or decreased the VprBP protein levels, respectively, with concomitant effects on HIV-1 replication. [score:4]
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[+] score: 8
miRNA-1236 inhibits HIV-1 infection of monocytes by repressing translation of cellular factor VprBP. [score:5]
Similarly, VprBP (Vpr binding protein), a cellular factor crucial for Vpr -mediated G2 cell-cycle arrest and proper viral replication, is targeted by hsa-miR-1236 (Ma et al., 2014). [score:3]
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9
[+] score: 6
Gao R, Cai C, Gan J, Yang X, Shuang Z, Liu M, et al. miR-1236 down-regulates alpha-fetoprotein, thus causing PTEN accumulation, which inhibits the PI3K/Akt pathway and malignant phenotype in hepatoma cells. [score:6]
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[+] score: 5
miR-1236 was a negative regulator of VEGFR-3 in lymphangiogenesis [28] and miR-181 was found to be an important regulator of angiogenesis and lymphangiogenesis via Prox-1 inhibition [29]. [score:5]
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[+] score: 5
Other miRNAs from this paper: hsa-mir-370, hsa-mir-373, mmu-mir-370, hsa-mir-1180
And we also proved that miR-1236, miR-1180 and miR-370 could activate the expression of suppressor gene p21 [34– 36]. [score:5]
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[+] score: 2
However, loci such as hsa-mir-1236 exhibit a typical pre-miRNAs with a 3' overhang, but still generate high frequency "xU" reads (Fig 7D). [score:1]
Amongst miRNAs annotated prior to 2012, the only pre-miRNA longer than 100 nt (i. e. the hairpin length inclusive of the cloned miRNA/star species) were the human loci mir-548o and mir-1236, and the mouse loci mir-3102, mir-702 and mir-1983. [score:1]
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[+] score: 2
Top three of them were positions 87 of hsa-miR-3151 and hsa-miR-4259, 1331 of hsa-miR-611, and 1478 of hsa-miR-1236. [score:1]
Besides the conserved start position 771, positions 139 of hsa-miR-1470, 141 of hsa-miR-3622a-3p, 148 of hsa-miR-485-3p, and 582 of hsa-miR-770-5p were highly conserved among more than one thousand sequences of NS1 genes in type 1 while position 137 was predicted start binding position of both hsa-miR-1236 and hsa-miR-1249. [score:1]
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[+] score: 1
The chromosomes HSCHR6_MHC_COX, HSCHR6_MHC_MANN, HSCHR6_MHC_DBB, HSCHR6_MHC_MCF, HSCHR6_MHC_QBL containing hsa-mir-219-1, HSCHR6_MHC_COX, HSCHR6_MHC_DBB, HSCHR6_MHC_MCF, HSCHR6_MHC_MANN, HSCHR6_MHC_QBL, HSCHR6_MHC_SSTO containing hsa-mir-877, HSCHR6_MHC_COX, HSCHR6_MHC_DBB, HSCHR6_MHC_MCF, HSCHR6_MHC_QBL, HSCHR6_MHC_SSTO containing hsa-mir-1236, and MT containing hsa-mir-1974, hsa-mir-1977 and hsa-mir-1978 as mentioned in the miRBase have been discarded. [score:1]
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[+] score: 1
Three of the human RBPs were removed from the dataset: microRNA 1236 (MIR1236; because it is a microRNA gene rather than an RBP), poly(A) binding protein, cytoplasmic 4 (PABPC4; the consensus was AAAAAAA, making normalization for dinucleotide composition impossible) and peptidylprolyl isomerase E (cyclophilin E) (PPIE; the consensus was WWWWWW, making it once again impossible to generate simulants). [score:1]
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