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34 publications mentioning mmu-mir-217

Open access articles that are associated with the species Mus musculus and mention the gene name mir-217. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 294
In pancreatic cancer [8], hepatocellular carcinoma [9], renal cell carcinoma [10] and chronic myelogenous leukemia [11], miR-217 is downregulated and functions as a tumor suppressor, while it overexpressed and acts as an oncogene in B-cell lymphomas [12]. [score:8]
Ectopic expression of miR-217 resulted in significant AEG-1 downregulation at both the mRNA and protein levels, whereas miR-217 silencing led to restoration of AEG-1 expression. [score:8]
In addition, our results indicate that miR-217 may suppress the tumorigenesis and aggressiveness of CRC through directly targeting AEG-1. Importantly, our findings implicate miR-217 as a prognostic marker and potential target for miRNA -based CRC therapy. [score:8]
To further clarify this point, we performed a rescue experiment which demonstrated that AEG-1 overexpression significantly reversed miR-217 -induced apoptosis, cell cycle arrest, proliferative inhibition and invasive suppression of SW620 cells. [score:7]
To clarify the underlying molecular mechanism of the suppressive effects of miR-217 on the proliferation and invasive capacity of CRC cells, we used bioinformatics methods (TargetScan, microRNA and miRDB) to search for potential target genes of miR-217. [score:7]
Furthermore, our study revealed, for the first time, the involvement of miR-217 in tumorigenesis through targeting AEG-1 targeting and that decreased miR-217 expression correlated with poor prognosis in patients with CRC. [score:7]
Interestingly, ectopic miR-217 expression decreased AEG-1 expression and repressed luciferase reporter activity associated with the AEG-1 3′-untranslated region (UTR). [score:7]
In 2009, Stuckenholz et al. [14] identified a number of novel genes, including miR-217, involved in mammalian gastrointestinal development, which were implicated as potential targets for therapeutic intervention in the management of gastrointestinal disease and cancer. [score:6]
In this study we show that miR-217 is significantly downregulated in CRC and that decreased miR-217 expression levels indicate poor prognosis of CRC patients. [score:6]
Fig. 6AEG-1 is upregulated in CRC tissues and negatively correlated with the expression level of miR-217 in both CRC and CRN tissue samples. [score:6]
Finally, in a nude mouse xenografted tumor mo del, miR-217 overexpression significantly suppressed CRC cell growth. [score:5]
Rescue of miR-217 ectopic expression effects by simultaneous overexpression of AEG-1. (A) Cell proliferation detected in SW620 cells at 1, 2, 3, 4 and 5 days after transfection. [score:5]
Moreover, our in vivo studies confirmed that miR-217 overexpression remarkably suppressed CRC xenograft tumor growth in nude mice. [score:5]
To elucidate the mechanism by which miR-217 expression affects cell proliferation, flow cytometry was employed to analyze the effects of miR-217 overexpression on CRC cell line apoptosis and cell cycle progression. [score:5]
In contrast, treatment with the miR-217 inhibitor caused an increase in AEG-1 mRNA and protein expression (Fig.   5d). [score:5]
Fig. 4Ectopic miR-217 expression inhibits invasion of SW480 and SW620 cells. [score:5]
Prediction software (TargetScan, microRNA and miRDB) analysis indicated that astrocyte -elevated gene-1 (AEG-1) is a potential target of miR-217. [score:5]
Similar to overexpression of miR-217, AEG-1 silencing markedly suppressed cell proliferation, colony formation, and invasive capacity, while G0/G1 arrest, and apoptosis were promoted (Additional file 3: Figure S2b-f). [score:5]
Furthermore, the expression level of AEG-1 was inversely correlated with the miR-217 expression in both CRC and CRN tissues. [score:5]
Moreover, knockdown of AEG-1 repressed cell growth and invasion, induced G0/G1 arrest and apoptosis, which was similar to the effects of miR-217 overexpression. [score:4]
These data indicate that miR-217 directly targets its predicted AEG-1 seed region. [score:4]
As shown in Fig.   5c, transfection of CRC cells with miR-217 mimics led to a remarkable downregulation in AEG-1 mRNA and protein levels. [score:4]
In our study, qRT-PCR analysis demonstrated that miR-217 was significantly downregulated in CRC tissue samples and cancer cell lines. [score:4]
MiR-217 suppressed AEG-1 expression by binding to its 3′UTR sequence. [score:4]
MiR-217 expression was deemed to be high when the expression level was equal to or above the median of the cohort and low when it was below the median of the cohort [26]. [score:4]
CRC cell lines with miR-217 upregulation and AEG-1 silencing were established and the effects on tumor growth in vitro and in vivo were assessed. [score:4]
MiR-217 overexpression significantly inhibited proliferation, colony formation and invasiveness of CRC cells by promoting apoptosis and G0/G1 phase arrest. [score:4]
In this study, we also showed, for the first time, that overexpression of miR-217 significantly repressed CRC cell proliferation, colony formation, and induced G0/G1 cell cycle arrest and apoptosis. [score:3]
The relationship between miR-217 expression and the clinicopathologic features of CRC was analyzed using the Pearson χ [2] test. [score:3]
In the present study, we focused on miR-217, which is abnormally expressed in a variety of cancer types [8– 10, 12]. [score:3]
These results demonstrate that lower miR-217 expression levels indicate poorer prognosis in CRC patients. [score:3]
Fig. 3Overexpression of miR-217 enhances apoptosis and promotes G0/G1 phase arrest in CRC cells. [score:3]
Our findings suggest that miR-217 has considerable value as a prognostic marker and potential therapeutic target in CRC. [score:3]
Using bioinformatics analysis, we found that miR-217 targeted multiple cancer-related genes that have been reported to have a close link with cancers, such as KRAS (pancreatic cancer) [8], E2F3 (hepatocellular carcinoma) [9], and DACH1 (breast cancer) [38]. [score:3]
Moreover, Kaplan–Meier analysis revealed that CRC patients with low miR-217 expression had a significantly shorter median survival (19.5 ± 2.9 vs. [score:3]
As shown in Fig.   2a, after transfection with miR-217 mimics, a 19.46-fold and 14.89-fold increase in miR-217 expression was observed in SW480 and SW620 cells, respectively. [score:3]
To date, the evidence for aberrant expression of miR-217 in CRC has been obtained in microarray studies. [score:3]
As shown in Additional file 4: Figure S3, overexpression of both miR-217 and AEG-1 in SW620 cells caused no significant effects on cell proliferation, invasive capacity, cell cycle and apoptosis. [score:3]
Fig. 1Determining miR-217 expression in CRC tissues and cell lines and its clinical significance. [score:3]
The final concentration of miR-217 mimics or inhibitor or siRNA-AEG1 was 50 nM. [score:3]
The average gene expression from NCM460 was appointed as 1. (c) Kaplan-Meier survival curve for CRC patients with miR-217 -high (n = 24) and miR-217-low (n = 26) character. [score:3]
AEG-1 silencing resulted in similar biological behavior changes to those associated with miR-217 overexpression. [score:3]
CRC cells were collected at 48 h after treatment with 50 nM miR-217 mimics or inhibitor or siRNA-AEG1 and corresponding controls. [score:3]
These results demonstrate that ectopic expression of miR-217 promotes apoptosis and G0/G1 phase arrest. [score:3]
These results imply that miR-217 acts as an inhibitor of colorectal tumorigenesis. [score:3]
The results showed that after overexpression of miR-217, the invasion capability of CRC cells was significantly reduced, indicating the involvement of miR-217 in CRC invasion and metastasis. [score:3]
Moreover, analysis of clinical data indicated that reduced expression of miR-217 in CRC patients correlated with poor tumor differentiation. [score:3]
In addition, Cox’s multivariate analysis indicated that miR-217 expression, TNM stage and distant metastasis act as an independent factor in the prediction of overall survival among patients with CRC. [score:3]
Therefore, the results indicate that decreased AEG-1 expression represents a mechanism by which miR-217 plays a role in the progression of cancer. [score:3]
Furthermore, Cox’s multivariate analysis showed that miR-217 expression, TNM stage and distant metastasis were significantly related to overall survival of CRC patients as independent prognostic factors (Table  2). [score:3]
We further evaluated the expression levels of AEG-1 mRNA and protein after modulation of miR-217 expression. [score:3]
Interestingly, Pearson correlation analysis revealed an obvious inverse correlation was observed between miR-217 and AEG-1 expression both in CRC tissues (r = −0.3457, P < 0.05) and in CRN tissues (r = −0.2944, P < 0.05) (Fig.   6b). [score:3]
These results indicate that miR-217 suppressed proliferation of CRC cell lines both in vitro and in vivo. [score:3]
Moreover, decreased miR-217 expression was also associated with shorter overall survival of CRC patients. [score:3]
32.0 ± 3.8 months, P = 0.032; Fig.   1C) than those with high miR-217 expression. [score:3]
Furthermore, all six CRC cell lines expressed lower levels of miR-217 than the normal colorectal cell line NCM460 (Fig.   1B). [score:3]
Interestingly, in this study, AEG-1 was predicted to be one of the target genes of miR-217. [score:3]
The clinical outcomes in the patients in this study revealed that the expression level of miR-217 was closely correlated with CRC distant metastasis and also acted as an independent prognostic factor in patients with CRC. [score:3]
We examined the expression of miR-217 and AEG-1 in 50 CRC tissues and the corresponding noncancerous tissues by qRT-PCR. [score:3]
All prediction analyses indicated that AEG-1 is a potential target of miR-217. [score:3]
To confirm the role of AEG-1 in the anti-cancer effects of miR-217 in CRC cells, we restored AEG-1 expression by AEG-1 plasmid transfection after transfection with miR-217 mimics. [score:3]
The SW480 and SW620 cell lines exhibited the lowest levels of miR-217 expression and were therefore, selected for use in subsequent studies. [score:3]
The correlation between miR-217 and AEG-1 expression in colorectal tissue samples. [score:3]
MiR-217 suppressed the CRC cell invasive activity. [score:2]
These results imply that miR-217 participates in the regulation of the CRC cell invasiveness. [score:2]
MiR-217 expression levels were closely correlated with tumor differentiation. [score:2]
qRT-PCR analysis showed that miR-217 expression was significantly decreased in CRC tissue samples compared with the corresponding CRN tissue samples (Fig.   1a). [score:2]
The present study compared the expression of miR-217 in CRC tissues and normal colorectal (CRN) tissues. [score:2]
MiR-217 -binding region of AEG-1 was identified by TargetScan 6.2 (http://www. [score:2]
qRT-PCR analysis showed that miR-217 expression levels were obviously increased in LV-miR-217-infected tumors compared with those in the control tumors (Fig.   2e). [score:2]
MiR-217 was involved in changes in the expression of molecules associated with invasion, cell cycle and apoptosis. [score:2]
The average miRNA expression from mimics NC was appointed as 1. (b) The proliferation curve of SW480 and SW620 cells after transfected with miR-217 mimics by CCK8 assay. [score:2]
The analysis of clinical pathological characteristics showed that low miR-217 expression was significantly associated with poor tumor differentiation (P = 0.038), but not with patient age, gender, tumor size, TNM stage, lymph node metastasis, or distant metastasis and vessel infiltration in CRC (Table  1). [score:1]
Based on these findings, we hypothesized that miR-217 plays a role in human CRC. [score:1]
Dual-luciferase reporter gene assays were also performed to investigate the interaction between miR-217 and AEG-1. Our data demonstrated that miR-217 was significantly downregulated in 50 pairs of colorectal cancer tissues. [score:1]
After cotransfection of SW480 cells with miR-217 mimics or NC mimics and AEG-1-UTR-WT or AEG-1-UTR-MUT plasmids, luciferase activity was analyzed. [score:1]
Recent studies have indicated the possible function of miR-217 in tumorigenesis. [score:1]
The histogram showed that miR-217 induced cell cycle arrest at G0/G1 phase. [score:1]
Moreover, the colonies formed by cells transfected with miR-217 mimics were obviously fewer in number and smaller in size than those formed by the control cells (Fig.   2c). [score:1]
Our results showed that miR-217 significantly decreased the relative luciferase activity in the reporter containing the wild-type 3′UTR, whereas the luciferase activity of the mutant was unaffected (Fig.   5b). [score:1]
We next used dual-luciferase assays to determine whether miR-217 binds directly to the 3′UTR of AEG-1 mRNA. [score:1]
The clinical significance of miR-217 was analyzed. [score:1]
Clinicopathologic significance of miR-217 in CRC patients. [score:1]
However, the role of miR-217 in CRC remains to be elucidated. [score:1]
The lentiviral miR-217 (LV-miR-217) and empty lentiviral (LV-miR-NC) vectors were generated by Genechem Company (Shanghai, China) and were used to transfect CRC cells according to the manufacturer’s instructions. [score:1]
Moreover, miR-217 was demonstrated to modulate epithelia cell senescence in metabolic disorders [13]. [score:1]
Therefore, in the current study, we investigated AEG-1 as the target for miR-217 to further explore the effects of miR-217/AEG-1 signaling on CRC. [score:1]
Xenografted tumors in mice inoculated with LV-miR-217-infected SW480 cells grew much more slowly than those in mice inoculated with the LV-miR-NC (Fig.   2d). [score:1]
These findings implicate miR-217 as a novel prognostic marker in CRC. [score:1]
containing the AEG-1 3′UTR (0–1,500 bp) or mutated sequences plus 50 nM miR-217 mimics or negative control (NC) mimic according to the manufacturer’s instructions. [score:1]
However, the roles of miR-217 in colorectal cancer (CRC) are still largely unknown. [score:1]
Thus, it can be hypothesized that restoration of miR-217 in CRC might be a new therapeutic approach in CRC, especially in CRC with distant metastasis. [score:1]
miR-217 AEG-1 colorectal cancer proliferation invasion Colorectal cancer (CRC) is the third most common cancer and the fourth most common cause of cancer deaths globally, accounting for approximately 1.2 million new cases and 600,000 deaths each year [1]. [score:1]
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[+] score: 96
Our in silico analysis revealed that miR-216 and miR-217 potentially target many important genes that play critical roles during the pathogenesis of PC (Table 1); and the downregulation of miR-217 [45] and miR-216 [44] suggests their potential as tumor suppressors in PC by targeting downstream targets, particularly the Kras oncogene [43] and Janus kinase 2 [44]. [score:12]
At 30 weeks of age, the expression of miR-216 (p-value = 0.016), miR-217 (p-value = 0.0078), miR-150 (p-value =0.023), Let-7b (p-value = 0.031,) and miR-96 were significantly downregulated, whereas the expression of miR-146b (p-value = 0.0078), miR-205, (p-value - 0.0078), miR-21, miR-195 (p-value = 0.031), and miR-34c (p-value = 0.063) were significantly upregulated in KC animals compared to control animals (Figure 2B). [score:10]
The expression of miR-223, miR-483-3p (p-value = 0.01), 146b, 205 (p-value = 0.001), 221, 21 (p-value = 0.023), 195, 34c and miR-26a (p-value = 0.0078) were significantly upregulated, whereas the expression of miR-216, miR-141, miR-217, Let-7b (p-value = 0.001), and Let-150 (p-value = 0.01) were significantly downregulated in human PC tissues as compared to the cancer-adjacent normal tissues (Figure 3E). [score:10]
At 40 weeks of age, the expression of miR-216, miR-217, miR-223, miR-141, miR-483-3p (p-value = 0.031), miR-195, Let-7b (p-value = 0.063) and miR-96 were significantly downregulated; on the other hand, the expression of miR-21, miR-205, miR-146b (p-value = 0.031), and miR-34c (p-value = 0.063) were upregulated in KC mice compared to the control animals (Figure 2C). [score:10]
In addition to KC mice, we also observed a significant downregulation of miR-216 and miR-217 in human PC tissue (Figure 3E); these results are in agreement with earlier studies on human PC [38– 43] that show downregulation of miR-217 in 76.2% (16/21) of PC tissue as well as cell lines [43]. [score:7]
The panel of differentially expressed miRNAs were validated by real-time PCR using TaqMan assays, and the results were consistent with the data that showed up-regulation of miR-21, miR-221, miR-100 and miR-26a and down-regulation of miR-26b, miR-141, miR-96, miR483-3p, miR-216, and miR-217 in the KC compared to control mice (Figure 1A). [score:7]
The analysis for the KC animals compared to controls revealed that miR-150, miR-494, miR-138, miR-148a*, miR-216a, and miR-217 (p-value = 0.01) were significantly downregulated (Table 1), whereas, miR-146b, miR-205, miR-31, miR-192, and miR-21 (p-value = 0.01) were significantly upregulated (Table 2). [score:6]
We have shown that in tumor samples compared to normal samples, the majority of miRNAs (miR-216, miR-217, miR-100, miR-345, miR-141, miR-483-3p, miR-26b, miR-150, Let-7b, Let-195 and miR-96) were downregulated, and few were upregulated (miR-146b, miR-205, miR-31, miR-192, miR-194 21, miR-379, miR-431, miR-541, and miR-199b). [score:6]
Further, at 50 weeks of age, the expression of miR-216, miR-217, miR-345, miR-141, miR-483-3p, miR-26b, miR-96, Let-7b (p-value = 0.01), miR-100, miR-26a and miR-150 (p-value = 0.094) were further downregulated in KC animals compared to control mice (Figure 2D). [score:5]
Several studies have shown the abnormal expression of miRNAs including miR-21, Let-7b, miR-100, miR-217, and miR-216 in PC and have proposed them as candidates for early diagnosis and potential molecular targets [23, 24]. [score:5]
Both miR-216 and miR-217 act as potential tumor suppressors for PC by targeting the Kras oncogene [43]. [score:5]
The expression of pancreas-specific tumor suppressors miR-217 and miR-216 were unaltered at 10 weeks of age (presence of PanIN-Ia and Ib), but progressively decreased from 25 – 50 weeks of age as PanIN lesions progressed to PDAC. [score:5]
The expressions of miR-216 and miR-217 were also progressively reduced in KC mice, but the expressions of miR-21, miR-205, miR-146b, miR-34c, and miR-223 progressively increased (Figure 1A, 2A– 2D). [score:5]
However, no significant difference was observed in the expression of pancreas-specific miR-217 (Figure 2A). [score:3]
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[+] score: 71
Other miRNAs from this paper: mmu-mir-21a, mmu-mir-21b, mmu-mir-21c
The area under curve (AUC) values demonstrated that expression of both exosomal CRNDE-p and miR-217 demonstrated high sensitivity and specificity and clearly, distinguished CRC patients from benign diseases. [score:5]
In general, the CRNDE-p expression was higher and miR-217 expression was lower in the serum exosomes isolated from CRC patients than in healthy subjects. [score:5]
Figure 3(A) Relative expression of serum exosomal CRNDE-p and miR-217 in CRC patients (n = 410), adenoma patients (n = 58) and healthy volunteers (n = 175). [score:3]
Differential expression of CRNDE-p and miR-217 in serum exosomes from CRC patients, adenoma patients and health volunteers. [score:3]
Moreover, the AUC value for combined expression of serum exosomal CRNDE-p and miR-217 was markedly higher than either CRNDE-p, miR-217, CEA alone or combined CRNDE-p/CEA. [score:3]
Figure 2(A) Relative expression of CRNDE-p and miR-217 in exosomes isolated from the culture supernatants of normal human colon mucosal epithelial cell line NCM460 and human colorectal cancer cell lines, namely, HT-29, SW480, HCT-116, SW620, LoVo, SW48, DLD-1, Caco2 and HT-15 lines. [score:3]
These data suggested an inverse relationship between exosomal CRNDE-p (high) and miR-217 (low) expression in CRC cell lines. [score:3]
Note: The expression of CRNDE-p and miR-217 were quantified relative to cel-miR-39 by qRT-PCR. [score:3]
The association between clinicopathological features of CRC patients and the exosomal CRNDE-p and miR-217 levels is shown in Table 1. We observed high CRNDE-p and low miR217 in the serum exosomes correlated with advanced T-stages (T3 and T4), lymph node metastasis and clinical stages (III and IV) as shown in Table 1. However, there was no significant correlation between exosomal CRNDE-p and miR-217 expression with the age, gender and location of CRC patients. [score:3]
Differential expression of exosomal CRNDE-p and miR-217 from human CRC cell lines and. [score:3]
Then, the exosomal CRNDE-p and miR-217 expression was determined by qRT-PCR using NCODE CE SYBR GREEN MIRNA kit (Life Technologies, Carlsbad, Calif) according to manufacturer's instructions. [score:3]
Relative expression of serum exosomal CRNDE-p and miR-217 in CRC xenograft mice and sham controls (n = 6). [score:3]
Differential expression of exosomal CRNDE-p and miR-217 in serum exosomes from CRC patients, adenoma patients and health volunteers and ROC curve analysis. [score:3]
Next, we analyzed the expression of CRNDE-p and miR-217 in exosomes from normal human colon mucosal epithelial cell line NCM460 and multiple human colorectal cancer cell lines, namely, HT-29, SW480, HCT-116, SW620, LoVo, SW48, DLD-1, Caco2 and HT-15. [score:3]
The relative expression levels of CRNDE-p and miR-217 were normalized against cel-miR-39 by the comparative 2 [−ΔΔCt] method. [score:3]
Correlations of clinicopathological parameters and expression level of CRNDE and miR-217 in patients with CRC (n = 410). [score:3]
This demonstrated an inverse relationship between serum exosomal CRNDE-p and miR-217 in association with CRC. [score:1]
In this study, we analyzed serum exosomal CRNDE-p and miR-217 levels in subgroups of CRC patients to identify association with clinicopathological parameters such as clinical staging, tumor classification, and lymph node and distant metastasis. [score:1]
To confirm the diagnostic value of serum exosomal CRNDE-p and miR-217 in CRC, we performed ROC curve analysis and determined their cutoff values in CRC patients and health subjects. [score:1]
We observed high CRNDE-p and low miR-217 levels in exosomes released from CRC cells than in exosomes released from the control NCM460 cells by quantitative real-time-PCR (Figure 2A) and Northern blot (Figure 2B). [score:1]
This suggests that serum exosomal CRNDE-p and miR-217 levels were potential prognostic biomarkers for CRC patients. [score:1]
Therefore, our results suggested an inverse correlation between exosomal CRNDE-p and miR-217 in both human CRC cell lines and the CRC mice xenograft mo del. [score:1]
Next, we analyzed the exosomal CRNDE-p and miR-217 in CRC patients by qRT-PCR by normalizing to cel-miR-39 as an internal control. [score:1]
We observed high CRNDE-p (Figure 3A) and low miR-217 (Figure 3B) levels in the exosomes from the serum of CRC patients than in adenoma patients or healthy subjects. [score:1]
RNA isolation and detection of exosomal CRNDE-p and miR-217 by qRT-PCR. [score:1]
In conclusion, our study demonstrates that serum exosomal CRNDE-p and miR-217 levels in combination show diagnostic and prognostic potential for CRC. [score:1]
Conversely, miR-217 levels were aberrantly low in pre-chemotherapy serum samples, but high in post-chemotherapy samples. [score:1]
Since, miR-217 does not bind CRNDE-p in the exosomes, we hypothesized that CRNDE-p probably binds to miR-217 only in the intracellular environment. [score:1]
This suggested that the combination of CRNDE-p and miR-217 was a better diagnostic predictor than any applicated conventional tumor marker CEA. [score:1]
We observed low CRNDE-p (Figure 3B) and high miR-217 levels in post-chemotherapy samples than in pre-chemotherapy samples. [score:1]
We observed high CRNDE-p and low miR-217 levels in the serum exosomes from the CRC xenograft mice than in sham controls (Figure 2D). [score:1]
This suggested that the combined CRNDE-p/miR-217 had better diagnostic potential than either individual factors alone or combined CRNDE-p/CEA. [score:1]
CRNDE-p and miR-217 levels in exosomes from human CRC cell lines and. [score:1]
Conversely, exosomal miR-217 levels increased over time in the NCM460 cells, but remained constant in most CRC cell lines except DLD-1 cells (Figure 2C). [score:1]
We observed high CRNDE-p and low miR-217 in the serum exosomes from patients with tumor stage T3/T4, clinical stage III/IV, lymph node and distant metastasis than in patients with tumor stageT1/T2, clinical stage I/II and without lymph node and distant metastasis. [score:1]
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[+] score: 43
Up-regulation of miR-217 could decrease the expression of KRAS protein, thereby inhibiting tumour cell growth [39]. [score:8]
To further determine that the up-regulation of mmu-miR-712-3p, mmu-miR-511-5p and mmu-miR-217-5p was specific response to T. gondii infection, we compared the expression of these three miRNAs in mice infected with T. gondii to mice infected with P. berghei, P. yoelii, P. chabaudi, C. parvum, MHV, or S. aureus. [score:5]
The levels of the three miRNAs, mmu-miR-712-3p, mmu-miR-511-5p and mmu-miR-217-5p miRNAs, were found specifically up-regulated in plasma of mice after T. gondii infection. [score:4]
We report the evidence that three miRNAs, including mmu-miR-712-3p, mmu-miR-511-5p and mmu-miR-217-5p, are significantly up-regulated in the plasma of mice after T. gondii infection, which may lead to the discovery of novel biomarkers for T. gondii infection. [score:4]
Another over-expressed miRNA from the plasma of mice with T. gondii infection is mmu-miR-217-5p, which is known to be encoded by a gene located on chromosome 11. [score:3]
Figure 3 ROC curve analysis of the expression of plasma levels of mmu-miR-712-3p, mmu-miR-511-5p and mmu-miR-217-5p. [score:3]
Previous studies indicated that miR-217 may act as a tumour suppressor, as suggested from a study on renal cell carcinoma and pancreatic ductal adenocarcinoma [38, 39]. [score:3]
Three of those miRNAs (mmu-miR-712-3p, mmu-miR-511-5p and mmu-miR-217-5p) were prominently expressed in mice infected by both the RH and ME49 strains of T. gondii. [score:3]
The expression of the three miRNAs mmu-miR-712-3p, mmu-miR-511-5p and mmu-miR-217-5p were further assessed in a large number of mice infected with either RH or ME49 strain of T. gondii. [score:3]
The elevated expression of miRNAs was specific to T. gondiiinfectionWe further investigated if the three elevated circulating miRNAs in plasma, mmu-miR-712-3p, mmu-miR-511-5p and mmu-miR-217-5p, were host specific responses to T. gondii infection. [score:1]
Quantitative analysis of these miRNAs in a large set of plasma samples from mice showed that mmu-miR-712-3p, mmu-miR-511-5p and mmu-miR-217-5p were potentially useful for early stage diagnosis, with a satisfactory degree of sensitivity and specificity. [score:1]
Of these miRNAs, mmu-miR-712-3p, mmu-miR-511-5p and mmu-miR-217-5p were detected with the highest abundance (the average Ct values were 17.43, 27.45 and 26.08, respectively). [score:1]
We focused on the analysis of three miRNAs, mmu-miR-712-3p, mmu-miR-511-5p and mmu-miR-217-5p, which were detected abundantly in mice infected with the RH (Type I) and ME49 (Type II) strains of T. gondii. [score:1]
Scatter plots of plasma levels of mmu-miR-712-3p (A), mmu-miR-511-5p (B), and mmu-miR-217-5p (C) in mice infected with RH and ME49 strains of T. gondii (n = 20 each) and in healthy subjects (n = 20). [score:1]
Thus, the data collectively suggest that the elevated responses of mmu-miR-712-3p, mmu-miR-511-5p and mmu-miR-217-5p in T. gondii infected mice were parasite-specific. [score:1]
Figure 2 Validation of mmu-miR-712-3p, mmu-miR-511-5p and mmu-miR-217-5p in plasma samples (n = 60). [score:1]
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[+] score: 43
miR-21a-3p, miR-31-5p, miR-155-5p and miR-200c were upregulated while miR-217-5p, miR-802-5p, miR-375-5p and miR-216-5p were downregulated (Color figure online) Surprisingly, in upregulated mRNAs, it was not the classical pancreatic progenitor-related genes that changed the most. [score:10]
miR-21a-3p, miR-31-5p, miR-155-5p and miR-200c were upregulated while miR-217-5p, miR-802-5p, miR-375-5p and miR-216-5p were downregulated (Color figure online) Surprisingly, in upregulated mRNAs, it was not the classical pancreatic progenitor-related genes that changed the most. [score:10]
In our results, miR-21a, miR-31, miR-200c and miR-155 were upregulated and miR-217, miR-802, miR-375 and miR-216 were downregulated (Additional file 9: Table S5). [score:7]
Moreover in noncoding RNAs, miR-21a, miR-31 and miR-155 were upregulated and miR-217, miR-802 and miR-375 were downregulated in colonies along with a number of other miRNAs and lncRNAs. [score:7]
In downregulated miRNAs, miR-216a-3p/5p, miR-216b-3p/5p, miR-217-5p, miR-802-3p/5p and miR-375-3p lay on the top. [score:4]
AC Azevedo-Pouly, DS Sutaria, J Jiang, OA Elgamal, F Amari, D Allard, et al. miR-216 and miR-217 expression is reduced in transgenic mouse mo dels of pancreatic adenocarcinoma, knockout of miR-216/miR-217 host gene is embryonic lethal. [score:4]
miR-216/miR-217 were supposed to be reduced in pancreatic adenocarcinoma [37]. [score:1]
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[+] score: 40
We propose a mo del of autophagy regulation in MMCs under diabetic conditions in which upregulation of TGF-β and miR-192 cascade and subsequently increased Akt activation could lead to inhibition of autophagy mediated either directly by miR-192, miR-217 and other downstream miRNAs targeting some of the autophagy genes, or via transcriptional regulation of these genes due to phosphorylation and inhibition of FoxO3a activity by Akt activation (Fig.   7). [score:13]
Loss of miR-192 and hence decreased Akt activation with subsequent reduction in mTOR activity could also contribute to reversal of autophagy suppression observed in the diabetic miR-192- KO mice 15, 40. miR-217 targets the 3′UTR of FoxO3A in endothelial cells [52]. [score:5]
We have previously shown that miRNA circuits downstream of TGF-ß, which include miR-192 and miR-217, induce MC hypertrophy as a consequence of Akt activation and downregulation of PTEN [40]. [score:4]
Furthermore, some of these genes are down-regulated by oligonucleotide mimics of miRNAs downstream of TGF-β namely miR-192 and miR-217. [score:4]
Overall, these results indicate that autophagy gene expression is regulated by the TGF-β pathway in MMCs and one of the mechanisms involved could be through downstream miRNAs, namely miR-192 and miR-217. [score:4]
Autophagy gene expression is decreased in MMC treated with TGF-β and certain genes are decreased with miR-192 and miR-217 mimic oligonucleotides. [score:3]
We transfected MMCs with either NC or 217-M and observed that expression of Atg1, LC3 and Becn1 were significantly decreased by miR-217-M compared to NC (Fig.   5C). [score:2]
We previously reported that miR-217 is another miRNA induced by TGF-ß, miR-192 and diabetic conditions that are involved in the signaling cascade downstream of TGF-ß and miR-192 in MMCs and also regulates the pathogenesis of DN [40]. [score:2]
We have previously shown that miR-192 can mediate fibrotic effects of TGF-ß and plays a key role in the pathogenesis of DN in MC 37, 38. miR-192 is also part of a cascade of downstream miRNAs (including miR-200, miR-216a, miR-217) that also regulate fibrotic genes and contribute to the pathogenesis of DN 39, 40. [score:2]
miR-192 mimics (192-M), miR-217 mimics (217-M), negative control oligonucleotides (NC) were obtained from Dharmacon (Lafayette, CO). [score:1]
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[+] score: 29
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, mmu-mir-98, 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, 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
MiR-217 was up-regulated by TGF-β and was able to activate Akt through the down-regulation of PTEN to increase glomerular mesangial cell survival and hypertrophy [52]. [score:6]
Ssc-miR-216 and ssc-miR-217 were also located in the same genome loci in chromosome 3. Overexpression of has-miR-216a/217 activates the PI3K/Akt and TGF-β signaling pathways by targeting PTEN and SMAD7 in human hepatocellular carcinoma cells [54]. [score:5]
Ssc-miR-182, ssc-miR-187, ssc-miR-136, ssc-miR-210, ssc-miR-217 and ssc-miR-10b participate in regulation Neurotrophin signaling pathway by targeting corresponding genes, including BNDF, SHC4, KRAS and FOXO3. [score:4]
NR4A2 was also targeted by has-miR-302d and has-miR-371, which indicates that miR-217 has some regulatory functions in common with other pluripotency -associated miRNAs in hESCs [53]. [score:4]
We also assessed another three selected miRNAs, ssc-miR-136, ssc-miR-217 and ssc-miR-182, which were found to be more highly expressed in mpiPSCs (Fig 3C). [score:3]
Additionally, ssc-miR-216, ssc-miR-217, ssc-miR-142-5p, ssc-miR-96-5p, ssc-miR-182 and ssc-miR-183 have higher expression levels in mpiPSCs than that in hpiPSCs (Fig 3A). [score:3]
However, miR-217 was found to target NR4A2 in hESCs to block differentiation. [score:3]
Interestingly, the mpiPSCs were characterized by high expression of miR-217. [score:1]
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[+] score: 18
For example, the mature miR-217-5p sequence is 5′TACTGCATCAGGAACTGACTGG-3′ and the isomiR-217-5p sequence 5′-TACTGCATCAGGAACTGACTGGAC-3′ are both highly enriched in the pancreas, but the miR-217-5p isomiR lacks expression in the stomach, intestine and ovary while other isomiRs of miR-217-5p are expressed in the stomach, intestine and ovary (see the last miR-217-5p isomiR in Additional file 10: Figure S2). [score:5]
Eli Lilly investigated the isomiR expression of pancreas tissue specific and enriched miRNAs and the analysis revealed that isomiRs generally mirror their parent miRNA expression (Additional file 10: Figure S2), but some isomiRs are more tissue specific than others as shown for miR-215 in the intestines (Additional file 11: Figure S3) and miR-217-5p in the pancreas (Additional file 10: Figure S2). [score:3]
IsomiRs of miR-217-5p display more expanded or restricted expression with respect to tissues. [score:3]
Amylase and lipase increases were noted from 1–8 h in rats in both 15 and 50 μg/kg dose groups while pancreatic necrosis was noted at 8, 24 and 48 h. MiR-375-3p has been reported to be enriched in islets and the miRNA with the highest intra-islet expression [38] and in our study was increased from 4–24 h in the 15 and 50 μg/kg groups, returning to approximately vehicle level by 48 h. MiR-216a-5p and miR-217-5p remained elevated in the serum of rats longer than amylase or lipase and had a much greater dynamic range which could be advantageous if detection of pancreatic injury is not able to be examined at earlier time points. [score:3]
MiR-216b displayed similar kinetics to miR-216a-5p, but with a reduced dynamic range while miR-217-5p displayed increases similar to amylase. [score:1]
MiR-216a-5p, amylase and lipase were increased in the serum concurrently at 1 h, remained elevated until 8 h while miR-216a-5p remained elevated until 24 h. MiR-217-5p displayed similar kinetics to miR-216a-5p except miR-217-5p generally had a larger dynamic range and remained elevated until 48 h. Both miRs-216a-5p and 217-5p displayed much larger dynamic ranges than amylase or lipase and remained elevated longer. [score:1]
MiR-216b-5p was increased in 1 vehicle treated animal and miR-217-5p was increased in 2 vehicle treated animals with no histopathologic or clinical chemistry correlates (data not shown). [score:1]
Interestingly, miR-217-5p displayed very large increases for the longest amount of time in the rat and this result was not reflected in the dog. [score:1]
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[+] score: 17
In addition, the frequencies of apoptosis -associated target genes of miR-192, miR-216a, and miR-217, all previously reported to be regulated by TGF-β in kidney disease [12- 14, 31], were not significantly different from random control miRNAs (Figure 2C). [score:6]
For example, extensive work has demonstrated that the upregulation of miR-192 [12] and miR-216a/miR-217 [14] by TGF-β in mesenchymal glomerular mesangial cells can switch off E-Box transcriptional repressors, resulting in increased collagen synthesis [12], and turn on Akt by repressing its inhibitor, PTEN, promoting mesangial cell survival and hypertrophy [14]. [score:6]
C. Bar graph shows the fraction of genes annotated with the biological process, ‘apoptosis’ (Ingenuity Systems), among all the predicted target genes of TGF-β-regulated miR-30s, miR-192, miR-216a, and miR-217 or the mean ± S. D. of 20 randomly chosen miRs that are not known to be regulated by TGF-β (control). [score:5]
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[+] score: 8
Wei R Deng Z Su J miR-217 targeting Wnt5a in osteosarcoma functions as a potential tumor suppressorBiomed. [score:5]
Recently, studies have shown that WNT5A (long isoform) is a target of several miRNAs, including miR-26a [47], miR-217 [48], miR-374 [49], and miR-590-5p [50]. [score:3]
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[+] score: 6
Other miRNAs from this paper: mmu-mir-196a-1, mmu-mir-196a-2
It has also been demonstrated that the expression of miRNA-196a (miR-196a) is high in pancreatic ductal adenocarcinoma (PDAC) but low in CP and normal tissues, whereas miR-217 exhibits the opposite expression pattern [8]. [score:5]
The ratio of miR-196a to miR-217 has been found to indicate whether tissue samples contain PDAC [9]. [score:1]
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[+] score: 6
In addition to tissue-specific ageing, it is increasingly evident that many miRNA regulate gene expressions in well-known ageing pathways, most notably in the p53 tumor suppressor pathway (miR-34, miR-29 and miR-217, etc. ) [score:6]
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[+] score: 6
ZFP488 is a transcription factor involved in oligodendrocyte differentiation and is targeted by four estrogen -downregulated miRNAs (miR-93-5p, miR-217-3p, miR-665-5p, and miR-3072-5p) [68]. [score:6]
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[+] score: 6
Further, miR-216a and miR-217, both of which target PTEN, activate Akt through PTEN down-regulation in kidney disorders [61]. [score:6]
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[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-127, mmu-mir-128-1, mmu-mir-132, mmu-mir-133a-1, mmu-mir-188, mmu-mir-194-1, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-mir-206, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-30e, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-211, hsa-mir-212, hsa-mir-214, hsa-mir-217, hsa-mir-200b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-127, hsa-mir-138-1, hsa-mir-188, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-31, mmu-mir-351, hsa-mir-200c, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-200c, mmu-mir-212, mmu-mir-214, mmu-mir-26a-2, mmu-mir-211, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-138-1, mmu-mir-128-2, hsa-mir-128-2, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-412, mmu-mir-431, hsa-mir-431, hsa-mir-451a, mmu-mir-451a, mmu-mir-467a-1, hsa-mir-412, hsa-mir-485, hsa-mir-487a, hsa-mir-491, hsa-mir-503, hsa-mir-504, mmu-mir-485, hsa-mir-487b, mmu-mir-487b, mmu-mir-503, hsa-mir-556, hsa-mir-584, mmu-mir-665, mmu-mir-669a-1, mmu-mir-674, mmu-mir-690, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-696, mmu-mir-491, mmu-mir-504, hsa-mir-665, mmu-mir-467e, mmu-mir-669k, mmu-mir-669f, hsa-mir-664a, mmu-mir-1896, mmu-mir-1894, mmu-mir-1943, mmu-mir-1983, mmu-mir-1839, mmu-mir-3064, mmu-mir-3072, mmu-mir-467a-2, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-467a-3, mmu-mir-669a-6, mmu-mir-467a-4, mmu-mir-669a-7, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-669a-8, mmu-mir-669a-9, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-669a-10, mmu-mir-467a-9, mmu-mir-669a-11, mmu-mir-467a-10, mmu-mir-669a-12, mmu-mir-3473a, hsa-mir-23c, hsa-mir-4436a, hsa-mir-4454, mmu-mir-3473b, hsa-mir-4681, hsa-mir-3064, hsa-mir-4436b-1, hsa-mir-4790, hsa-mir-4804, hsa-mir-548ap, mmu-mir-3473c, mmu-mir-5110, mmu-mir-3473d, mmu-mir-5128, hsa-mir-4436b-2, mmu-mir-195b, mmu-mir-133c, mmu-mir-30f, mmu-mir-3473e, hsa-mir-6825, hsa-mir-6888, mmu-mir-6967-1, mmu-mir-3473f, mmu-mir-3473g, mmu-mir-6967-2, mmu-mir-3473h
Furthermore, the pathway analysis links a group of miRNAs that were differentially expressed in cbs [+/–] retina to oxidative stress pathway such as miR-205, miR-206, miR-217, miR-30, miR-27, miR-214 and miR-3473. [score:3]
Other miRNAs were linked to the hypoxia signaling pathway, for instance, miR-205, miR-214, miR-217, miR-27, miR-29, miR-30 and miR-31. [score:1]
Hcy also induces alteration of miRNAs related to tight junctions signaling such as miR-128, miR-132, miR-133, miR-195, miR-3473, miR-19, miR-200, miR-205, miR-214, miR-217, miR-23, miR-26, miR-29, miR-30, miR-31 AND miR-690. [score:1]
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[+] score: 5
Other miRNAs from this paper: mmu-mir-155, mmu-mir-181b-1
In accordance with spontaneous GC formation, the array analysis showed an upregulation of two genes encoding miRs associated with the GC reaction: miR-155 31, 32 and miR-217 [33]. [score:4]
Interestingly, we found increased transcript levels of miRs, which coordinate GC formation, CSR/SHM, PC differentiation, and memory B cell differentiation, such as miR-155 [31] and miR-217 [33]. [score:1]
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[+] score: 5
Recent studies have suggested important regulatory roles for miRNAs such as miR-21, miR-216, miR-217, miR-181b, miR-31b and miR-34a, which were confirmed to be upregulated in senescing HUVECs (Menghini et al., 2009), and miR-146, miR-142-3p, miR-223 and miR-29 family members, which were significantly increased in whole aortas of aged mice (Zhao et al., 2010). [score:5]
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[+] score: 4
However, an interesting aspect of using miR-148a is that it has been proposed as one of the three miRNAs (together with miR-217 and miR-375) which downregulation is a signature of PDAC [22]. [score:4]
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[+] score: 4
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-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-28, hsa-mir-29b-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-145a, mmu-mir-150, mmu-mir-10b, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-217, hsa-mir-218-1, hsa-mir-223, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-150, hsa-mir-195, hsa-mir-206, 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-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-22, mmu-mir-29c, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-331, mmu-mir-331, rno-mir-148b, mmu-mir-148b, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-28a, mmu-mir-200c, mmu-mir-218-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-29c, hsa-mir-200a, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-135b, hsa-mir-148b, hsa-mir-331, 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-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-10a, rno-mir-10b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-22, rno-mir-28, rno-mir-29b-1, rno-mir-29c-1, rno-mir-124-3, rno-mir-124-1, rno-mir-124-2, rno-mir-133a, rno-mir-143, rno-mir-145, rno-mir-150, rno-mir-195, rno-mir-199a, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-206, rno-mir-217, rno-mir-223, dre-mir-7b, dre-mir-10a, dre-mir-10b-1, dre-mir-217, dre-mir-223, hsa-mir-429, mmu-mir-429, rno-mir-429, mmu-mir-365-2, rno-mir-365, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-145, dre-mir-150, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-let-7j, dre-mir-135b, rno-mir-1, rno-mir-133b, rno-mir-17-2, mmu-mir-1b, dre-mir-429b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-133c, mmu-mir-28c, mmu-mir-28b, hsa-mir-451b, mmu-mir-195b, mmu-mir-133c, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, rno-let-7g, rno-mir-29c-2, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
Cortex let-7c-1, miR-10a, miR-21, miR-124a-1, miR-128a, miR-135b, miR-150, miR-199a, miR-217, miR-329, miR-451. [score:1]
Hypothalamus miR-17, miR-29c, miR-124a-1, miR-128a, miR-150, miR-199a, miR-217, miR-223, miR-329, miR-429. [score:1]
Olfactory bulb let-7b, let-7c-1, let-7c-2, miR-10a, miR-16, miR-17, miR-21, miR-22, miR-28, miR-29c, miR-124a-1, miR-124a-3, miR-128a, miR-135b, miR-143, miR-148b, miR-150, miR-199a, miR-206, miR-217, miR-223, miR-29b-1, miR-329, miR-331, miR-429, miR-451. [score:1]
Spinal cord miR-28, miR-217, miR-218-1, miR-329, miR-331. [score:1]
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[+] score: 3
Recently, Ramiro et al. found that overexpression of miR-217 in B cells enhances T cell -dependent immunization responses by improving the efficiency of GC formation, CSR, and SHM, as well as the generation of plasma and terminally differentiated memory B cells [6]. [score:3]
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[+] score: 3
In recent years, several miRNAs, such as miR-155 [32], and miR-217 [33], related fat liver disease have been identified. [score:3]
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[+] score: 3
Other recent studies have reported that miR-9, miR-101 and miR-217 target MALAT1 for degradation in other human cancer cell lines. [score:3]
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[+] score: 3
Previous studies have reported that miR-216a, miR-216b, and miR-217 are specifically expressed in the pancreas; these miRNAs were useful as biomarkers for pancreatic injury [30]. [score:3]
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[+] score: 3
MiRNAs have been found to regulate cell proliferation, differentiation, and apoptosis [15- 17] and they have also been implicated in the regulation of senescence (miR-29, miR-30, miR-34a, miR-34b, miR-34c, miR122 miR-203, miR-205 and miR-217) [18- 23] mostly by interfering with either the p53 pathway or the retinoblastoma RB1/E2F function. [score:3]
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[+] score: 3
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-98, 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, 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 previous study showed that runx2 is a target of miR-30c, miR-135a, miR-204, miR-133a, miR-217, miR-205, miR-34, miR-23a and miR-338 [34]. [score:3]
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[+] score: 2
We selected 14 of these miRs which might have been involved in regulation of angiogenesis, including miR-17-5p, miR-19a, miR-23a, miR-24, miR-31, miR-34a, miR-126, miR-130a, miR-132, miR-16, miR-21, miR-217, miR-221, and miR-378 for our study. [score:2]
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[+] score: 2
Other miRNAs from this paper: mmu-mir-122, hsa-mir-217, hsa-mir-122, dre-mir-217, dre-mir-122
microRNAs (miR-217 and miR-122), tight junction protein claudin C, FAM136a, and zebrafish tetraspanin, are involved the process of gastrointestinal development. [score:2]
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[+] score: 2
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-22, hsa-mir-25, hsa-mir-33a, hsa-mir-96, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-141, mmu-mir-155, mmu-mir-10b, mmu-mir-129-1, mmu-mir-181a-2, mmu-mir-183, mmu-mir-184, hsa-mir-192, mmu-mir-200b, hsa-mir-129-1, mmu-mir-122, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-183, hsa-mir-210, hsa-mir-181a-1, hsa-mir-216a, hsa-mir-217, hsa-mir-223, hsa-mir-200b, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-122, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-141, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-129-2, hsa-mir-184, mmu-mir-192, 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-22, mmu-mir-96, mmu-mir-34a, mmu-mir-129-2, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-155, mmu-mir-10a, mmu-mir-25, mmu-mir-210, mmu-mir-181a-1, mmu-mir-216a, mmu-mir-223, mmu-mir-33, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-200a, hsa-mir-34b, hsa-mir-34c, hsa-mir-375, mmu-mir-375, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, hsa-mir-33b, mmu-mir-216b, hsa-mir-216b, mmu-mir-1b, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, mmu-mir-129b, mmu-mir-216c, bbe-let-7a-1, bbe-let-7a-2, bbe-mir-10a, bbe-mir-10b, bbe-mir-10c, bbe-mir-125a, bbe-mir-125b, bbe-mir-129a, bbe-mir-129b, bbe-mir-133, bbe-mir-1, bbe-mir-183, bbe-mir-184, bbe-mir-200a, bbe-mir-200b, bbe-mir-210, bbe-mir-216, bbe-mir-217, bbe-mir-22, bbe-mir-252a, bbe-mir-252b, bbe-mir-278, bbe-mir-281, bbe-mir-33-1, bbe-mir-33-2, bbe-mir-34a, bbe-mir-34b, bbe-mir-34c, bbe-mir-34d, bbe-mir-34f, bbe-mir-375, bbe-mir-7, bbe-mir-71, bbe-mir-9, bbe-mir-96, bbe-mir-34g, bbe-mir-34h, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
In contrast, many phylogenetically conserved miRNAs, as well as miRNAs present in both chordates and vertebrates (for example, miR-216, miR-217, miR-22, miR-25, and miR-96), could be reliably traced back to B. belcheri (Gray). [score:1]
Based on the available nematode, fruitfly, zebrafish, frog, chicken, mouse, rat and human miRNA information [18], 45 conserved amphioxus miRNAs could be classified into three distinct groups: 23 miRNAs (let-7a, miR-1, miR-7, miR-9, and so on) were conserved throughout the Bilateria; 5 miRNAs (miR-252a, miR-252b, miR-278, miR-281 and miR-71) were homologous to invertebrate miRNAs; and 17 miRNAs (miR-141, miR-200a, miR-200b, miR-183, miR-216, miR-217, miR-25, miR-22, miR-96, and so on) were present both in chordates and vertebrates (Table S9 in). [score:1]
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[+] score: 2
Previous study reported that miR-216 and miR-217 promoted TGF β -induced MC hypertrophy in vitro by regulating PTEN 32. [score:2]
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[+] score: 1
Other miRNAs from this paper: hsa-mir-216a, hsa-mir-217, mmu-mir-216a, gga-mir-216a, gga-mir-217
The other variants with shorter 3′UTRs, however, loose between 16 and 36 potential miRNA binding sites, and among these are the experimentally validated binding sites of miR-216a and miR-217. [score:1]
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[+] score: 1
Other miRNAs from this paper: mmu-mir-146a
Furthermore, decreased levels of certain miRNAs such as miRNA-217 and miRNA-146a have been demonstrated to modulate senescence of endothelial cells in vitro [67], [68]. [score:1]
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[+] score: 1
They determined that TGF- β activates Akt in glomerular mesangial cells by inducing miR-215a and miR-217, revealing a role for miRNAs in kidney disorders. [score:1]
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[+] score: 1
However, ISH detection of other retina-specific miRs, including miR-213, miR-216, and miR-217, was unsuccessful in retina [26, 27]. [score:1]
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[+] score: 1
To date only few lncRNAs have been reported as hosts for some miRNAs under diabetic conditions, for e. g., RP23-298H6.1-001 hosting miR-216a and miR-217 (refs 6, 11, 28, 29, 30). [score:1]
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