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25 publications mentioning hsa-mir-572

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-572. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 276
Furthermore, we demonstrate that miR-572 directly targets and downregulates SOCS1 and p21 via recognizing their 3` UTRs, and downregulation of SOCS1 or p21 was essential for the miR-572 -mediated effects in ovarian cancer cells. [score:10]
In conclusion, miR-572 is overexpressed in ovarian cancer and upregulation of miR-572 promoted ovarian cancer cell proliferation, cell-cycle progression and tumorigenicity both in vitro and in vivo, while inhibition of miR-572 lead to the opposite effects. [score:8]
In the present study, SOCS1 and p21 were both identified as direct targets of miR-572 and could be suppressed by overexpression of miR-572, which in turn increased the proliferation and cell cycle progression of ovarian cancer cells in vitro and promoted tumorigenesis in an in vivo mo del of ovarian cancer. [score:8]
showed that ectopic expression of miR-572 dramatically decreased, whereas inhibition of miR-572 increased, the protein expression levels of SOCS1 and p21 in both S KOV3 and OVCAR3 ovarian cancer cells (Figure 5B). [score:7]
Our study demonstrates that miR-572, which is overexpressed in human ovarian cancer, can target and suppress both SOCS1 and p21, leading to ovarian cancer progression. [score:7]
Additionally, the expression of miR-572 correlated with ovarian cancer progression and overall patient survival, indicating that upregulation of miR-572 may contribute to the development of ovarian cancer and may have potential as a diagnostic and prognostic biomarker for ovarian cancer. [score:7]
Meanwhile, the expression of CyclinD1 was increased by ectopic expression miR-572, decreased by miR-572 inhibition (Figure 5B). [score:7]
As shown in Figure 5C, miR-572 significantly reduced the luciferase activity of the SOCS1 and p21 reporter genes, whereas transfection of the miR-572 inhibitor upregulated the luciferase activity of the reporter genes. [score:6]
These results suggest that downregulation of miR-572 inhibits proliferation, reduces tumorigenicity and prevents cell cycle progression in ovarian cancer cells. [score:6]
Moreover, the function of miR-572 in ovarian cancer may be exerted via downregulation of the target genes SOCS1 and p21, which play an important role in the function of miR-572 in ovarian cancer. [score:6]
Herein, we report that miR-572 is significantly upregulated in ovarian cancer and that the expression of miR-572 correlates with progression and overall survival in human ovarian cancer. [score:6]
Ovarian cancer cells stably expressing miR-572 formed higher numbers and larger colonies than the control cells, while inhibition of miR-572 led to the formation of fewer and smaller colonies (Figure 4A and 4B). [score:5]
These results suggest that miR-572 decreases the expression of SOCS1 and p21 and increases Cyclin D1 expression, consequently resulting in an aggressive phenotype and poorer prognosis in ovarian cancer (Figure 7). [score:5]
In an attempt to identify the mRNA targets of miR-572, we performed bioinformatic analysis using a publicly available algorithm (TargetScan 6.2). [score:5]
miR-572 is overexpressed in the serum of patients with nasopharyngeal carcinoma and renal cell carcinoma, and was used to construct a miRNA signature for patients prognosis [36, 37], and Li et al. found miR-572 was significantly overexpressed in peripheral T cell lymphoma, not otherwise specified (PTCL-NOS) [38]. [score:5]
The expression of the miRNA was defined based on Ct, and relative expression levels were calculated as 2−[(Ct of miR-572) -(Ct of U6)] after normalization with reference to the expression of small nuclear RNA U6. [score:5]
As shown in Figure 5G, silencing SOCS1 or p21 in miR-572 -inhibitor transfected cells also increased the mRNA and protein expression of Cyclin D1, a well-characterized regulator of cell proliferation. [score:4]
The evidence discussed above indicates that downregulation of SOCS1 and p21 may play essential roles in miR-572 -induced tumor progression in ovarian cancer. [score:4]
The level of DNA synthesis was also significantly suppressed in miR-572 -inhibited cells compared to control cells (Figure 3C). [score:4]
Proposed for mo del for the mechanism by which miR-572 -mediated downregulation of SOCS1 and p21 promotes ovarian cancer cell proliferation. [score:4]
miR-572 is upregulated in ovarian cancer. [score:4]
As shown in Figure 3A and 3B, suppression of miR-572 via transfection of the miR-572 inhibitor significantly decreased the growth rate of both ovarian cancer cell lines compared the respective negative control (miRZip-Vector) cells. [score:4]
Taken together, these results confirm that SOCS1 and p21 are direct targets of miR-572. [score:4]
Besides, consistent with our results, miR-572 was found upregulated in various malignancies [37, 38]. [score:4]
This study demonstrates that miR-572 plays an important role in the development and progression of ovarian cancer and may represent as a potential therapeutic target for ovarian cancer. [score:4]
Moreover, miR-572 was also reported downregulation in basal cell carcinoma [57]. [score:4]
Zhu et al. found significant downregulation of miR-572 in chronic lymphocytic leukemia [56]. [score:4]
miR-572 is upregulated and correlates with overall survival in human ovarian cancer. [score:4]
This study demonstrates that miR-572 is significantly upregulated in ovarian cancer. [score:4]
Expression of miR-572, SOCS1, p21 and Cyclin D1 in human ovarian cancer tissues. [score:3]
Expression of miR-572 was further examined in 108 archived clinical ovarian cancer specimens. [score:3]
Figure 7 (A) Real-time PCR analysis of miR-572 and Western blot analysis of SOCS1, p21 and Cyclin D1 expression in human ovarian cancer tissues. [score:3]
As shown in Figure 6A and 6B, the levels of miR-572 correlated with the protein expression levels of SOCS1 (r = −0.742, P = 0.022), p21 (r = −0.762, P = 0.017) and Cyclin D1 (r = 0.739, P = 0.023). [score:3]
Figure 6(A) Real-time PCR analysis of miR-572 and Western blot analysis of SOCS1, p21 and Cyclin D1 expression in human ovarian cancer tissues. [score:3]
To evaluate the effects of SOCS1 and p21 on miR-572 -induced ovarian cancer progression, we suppressed the expression of endogenous SOCS1 or p21 using specific siRNAs (Figure 5D). [score:3]
Figure 7 By analyzing a published microarray -based high-throughput assessment (NCBI/E-MTAB-1067), we found that miR-572 was upregulated significantly (P < 0.0001) in human ovarian cancer tissues compared to normal ovarian tissues (Figure 1A). [score:3]
Figure 5(A) Putative target sites for miR-572 in the 3` UTRs of SOCS1 and p21 and the sequence of miR-572 mutant (miR-572-mut). [score:3]
Luciferase reporter plasmids containing regions of the 3` UTR of SOCS1 or p21 were constructed and cotransfected into ovarian cancer cells with miR-572, miR-572 inhibitor or the corresponding negative controls. [score:3]
As shown in Figure 1B, miR-572 was expressed at low levels in stage I and II tumors, markedly increased in stage III tumors and was further elevated in stage IV ovarian cancer. [score:3]
The miR-572 anti-sense (miRZip-572) plasmid used as miR-572 inhibitor, and the vector control (miRZip-Vector) were purchased from System Biosciences (San Francisco, CA) and used according to previous report [31]. [score:3]
Inhibition of miR-572 reduces cell proliferation and cell-cycle progression in ovarian cancer cells. [score:3]
MicroRNA-572 directly suppresses SOCS1 and p21 in ovarian cancer cells. [score:3]
These results suggest that silencing SOCS1 or p21 in miR-572-repressed cells reversed the negative effect of the miR-572 inhibitor on ovarian cancer cell proliferation and tumorigenesis. [score:3]
This data suggests a possible link between high-level miR-572 expression and the progression of human ovarian cancer, and highlights miR-572 may have potential value as a prognostic biomarker in ovarian cancer. [score:3]
As shown in Figure 5A, SOCS1 and p21, which are critical attenuators of cell proliferation and cell-cycle progression, were identified as potential targets of miR-572. [score:3]
Next, loss-of-function studies using a miR-572 inhibitor (miRZip-572) were performed to confirm the biological function of miR-572 in ovarian cancer progression. [score:3]
Figure 1(A) Analysis of a public microarray data revealed that miRNA-572 was upregulated in human ovarian cancer tissues (n = 183) compared with normal ovarian tissues (n = 8; P < 0.0001; NCBI/E-MTAB-1067). [score:3]
In addition, flow cytometry revealed a significant increase in the percentage of cells in the G1/G0 phase and decrease in the percentage of cells in the S phase in miR-572 inhibited cells (Figure 3D). [score:3]
In agreement with these observations, upregulation of miR-572 was confirmed in 13 ovarian cancer cell lines compared with a control normal ovarian epithelial cell line (HOSEpiC; Figure 1E). [score:3]
Suppression of SOCS1 or p21 are required for miR-572 -induced cell proliferation and tumorigenesis in ovarian cancer. [score:3]
Overexpression of miR-572 promotes proliferation and cell cycle progression in ovarian cancer cells. [score:3]
Inhibition of miR-572 attenuates proliferation and cell cycle progression in ovarian cancer cells. [score:3]
Ectopic miR-572 promoted - while inhibition of miR-572 reduced - the proliferation, cell-cycle progression and tumorigenicity of ovarian cancer cells in vitro. [score:3]
Finally, to examine whether miR-572 -mediated suppression of SOCS1 and p21 in ovarian cancer is clinically relevant, seven freshly collected ovarian cancer samples and two normal ovarian tissues were obtained for further study. [score:3]
By analyzing a published microarray -based high-throughput assessment (NCBI/E-MTAB-1067), we found that miR-572 was upregulated significantly (P < 0.0001) in human ovarian cancer tissues compared to normal ovarian tissues (Figure 1A). [score:3]
However, miR-572 was downregulated in gastric cancer cell lines compared to normal gastric mucosa [55]. [score:3]
Therefore, this study demonstrates that miR-572 may play an important role in ovarian cancer progression and may represent a potential therapeutic target for ovarian cancer therapy. [score:3]
Kaplan-Meier analysis and the log-rank test indicated that a high level of miR-572 expression was associated with significantly shorter overall survival (P < 0.001; Figure 1C, Supplemental Table 2). [score:3]
Furthermore, cell cycle analysis showed ectopic overexpression of miR-572 significantly increased the percentage of cells in the S phase and decreased the percentage of cells in the G1/G0 peak (Figure 2D). [score:3]
MicroRNA-572 suppresses the tumorigenicity of ovarian cancer cells both in vitro and in vivo. [score:2]
MicroRNA-572 suppresses the tumorigenicity of ovarian cancer cells both in vitro and in vivoThe anchorage-independent growth assay was performed to examine the effects of miR-572 on the tumorigenicity of ovarian cancer cells. [score:2]
To investigate the biological function of miR-572 in the development and progression of ovarian cancer, S KOV3 and OVCAR3 ovarian cancer cells stably expressing miR-572 were established (Supplemental Figure 1). [score:2]
Figure 2(A) Effects of ectopic overexpression of miR-572 on the proliferation of the indicated ovarian cancer cell lines, as analyzed by the MTT assay. [score:2]
The MTT assay demonstrated that ectopic overexpression of miR-572 significantly increased the growth rate of both S KOV3 and OVCAR3 cells (Figure 2A). [score:2]
The colony formation assay revealed that ectopic overexpression of miR-572 markedly enhanced the growth ability of both S KOV3 and OVCAR3 cells, as indicated by increased colony numbers and sizes (Figure 2B). [score:2]
MiR-572 suppresses tumorigenicity of ovarian cancer cell both in vitro and in vivo. [score:2]
Real-time PCR analysis revealed that miR-572 was significantly overexpressed in 12 freshly-collected ovarian cancer samples compared to two normal ovarian tissues (Figure 1D). [score:2]
pMSCV-miR-572 was then cotransfected with the pIK packaging plasmid into 293FT cells, using the standard calcium phosphate transfection method [30]. [score:1]
The colony formation assay indicated that silencing SOCS1 or p21 increased the proliferation of ovarian cells transfected with the miR-572 inhibitor (Figure 5E); similar results were observed in the anchorage-independent growth assay (Figure 5F). [score:1]
As shown in Figure 4C-4E, the tumors formed by miR-572- transduced ovarian cancer cells were larger, in both size and weight, than the corresponding control tumors, whereas the tumors formed by miR-572- silenced ovarian cancer cells were smaller in size and weight than the corresponding control tumors. [score:1]
However, transfection of miR-572-mut (miR-572 mutant) had no significant effect on the luciferase activity of the reporter genes (Figure 5C); and miR-572 also had no effect on the luciferase activity of the mutant reporter genes (Supplemental Figure 3). [score:1]
Therefore, our results indicate the potential value of miR-572 in ovarian cancer development and miR-572 could be considered as useful biomarker for ovarian cancer diagnosis and prognosis. [score:1]
Clinical relevance of miR-572, SOCS1, p21 and Cyclin D1 in ovarian cancer. [score:1]
One group of mice was inoculated subcutaneously with S KOV3/Vector cells (5×10 [6]) in the left dorsal flank and with S KOV3/miR-572 cells (5×10 [6]) in the right dorsal flank per mouse. [score:1]
The Chi-squared test revealed that the levels of miR-572 strongly correlated with FIGO stage (P < 0.05; Figure 1B, Supplemental Table 2). [score:1]
Collectively, these results demonstrate that miR-572 functions to enhance proliferation and cell cycle progression in ovarian cancer cells. [score:1]
miR-572 promotes cell proliferation and cell-cycle progression in ovarian cancer cells. [score:1]
The expression of miR-572 in ovarian cancer has not previously been investigated. [score:1]
SOCS1 and p21 are essential for miR-572 -mediated proliferation in ovarian cancer. [score:1]
The biological effect of miR-572 on ovarian cancer progression was further examined using an in vivo tumor mo del. [score:1]
The miR-572-transduced ovarian cancer cells and miR-572-silenced cells, or the corresponding control cells, were subcutaneously injected into the dorsal flank of nude mice (Supplemental Figure 2). [score:1]
These data indicate that miR-572 plays a pivotal role in ovarian cancer progression in vivo. [score:1]
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2
[+] score: 80
Statistical analyses of our data revealed that 71 miRNAs out of 939 examined were expressed by this set of MSC lines at all passages and the expression of 11 miRNAs were significantly different between passages 3 and 7, while the expression of 7 miRNAs was significantly different between passages 3 and 5. The expression of these identified miRNAs was evaluated using for both the first set of MSC lines (n = 6) and a second set of MSC lines (n = 7) expanded from passages 4 to 8. By only 2 miRNAs, miR-638 and miR-572 were upregulated at passage 7 compared to passage 3 in the first set of MSC lines by 1.71 and 1.54 fold, respectively; and upregulated at passage 8 compared to passage 4 in the second set of MSC lines, 1.35 and 1.59 fold, respectively. [score:11]
The study revealed that the expression of miR-572 inhibited the targets of suppressor of cytokine signaling 1 (SOCS1) and p21 to promote cell proliferation and cell cycle progression of ovarian cancer cell lines, OVCAR3 and S KOV3. [score:9]
However in contrast, the gene, PPP2R2C, was identified as a target of miR-572 because its suppression by siRNA exhibited increased ovarian cell proliferation when miR-572 was also inhibited. [score:7]
While the expression of miR-572 and miR-638 was consistently observed to be statistically upregulated at later passages, the number of other statistically significant miRNAs varied between the microarray and platforms. [score:6]
MiR-638 which exhibited similar upregulation in expression at later passages as miR-572 in aging MSCs has been identified in a number of different carcinomas including colorectal, gastric, hepatocellular, nasopharyngeal, esophageal squamous cell, pancreatic adenocarcinoma, ovarian cancer and triple negative breast cancer [59, 64– 73]. [score:6]
These phenotypic changes may have corresponded with the gene expression differences observed between passages; therefore it is conceivable that some of these changes also correspond with the upregulation of miR-572 and miR-638 at later passages in MSCs. [score:6]
In our study, only miR-572 and miR-638 expression was observed to be significantly upregulated in two different sets of MSCs. [score:6]
By microarray analysis, 11 miRNAs were also observed to be significantly different between early and late passages; however, only two miRNAs, miR-572 and miR-638, were observed to be upregulated at later passages. [score:4]
In another study by Wu et al., several additional ovarian cancer cells lines were evaluated where upregulation in the expression of miR-572 promoted ovarian cancer cell proliferation [62]. [score:4]
Zhang et al. observed that miR-572 was upregulated in ovarian cancer and likely corresponded with cancer progression and overall patient survival [63]. [score:4]
The presented work has thoroughly shown that the expression of 2 miRNAs, miR-572 and miR-638, may be used to distinguish early and late passaged MSCs. [score:3]
Additionally, this research group also attempted to establish a MSC miRNA signature by identifying consistently expressed miRNAs where two on their list were miR-572 and miR-638. [score:3]
In the first set of MSCs, only miR-572 and miR-638 were observed to be significantly (p < 0.05) upregulated 1.54 and 1.71 fold, respectively, at passage 7 compared to passage 3 (Additional file 8: Table S5). [score:3]
The expression of miR-638 and miR-572 can distinguish MSCs from two different passages of cell culture. [score:3]
In contrast, for the second set of MSCs, 6 out of the 11 miRNAs (miR-196b-5p, miR-16-5p, miR-1202, miR-572, miR-638, and miR-15b-5p) evaluated for cellular aging were statistically significant (p < 0.05) between passage 4 and 8. miRNAs, miR-572 and miR-638 were significant in the second set of MSCs and upregulated at the later passage by 1.59 and 1.35, respectively. [score:2]
Based on the statistical significance of miRNAs miR-572 and miR-638 across two different platforms and using two different sets of MSCs, these results are likely to be highly replicable. [score:1]
In contrast, elevated miR-572 expression in MSCs at higher passages from our investigations corresponded with a lower capacity for proliferation. [score:1]
In addition, we identified 2 miRNAs (miR-572 and miR-638) that changed as a result of cellular passaging through in vitro expansion. [score:1]
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3
[+] score: 72
Some other target genes of miR-572 including CDKN1A, DICER1, WNT7A are also reported to be associated with vital neural functions, which might be down-regulated by fluoxetine -induced upregulation of miR-572 expression [37]. [score:11]
Up-regulated expression of miR-572 (ΔΔCt = 2.161, p = 4.58E-06) and miR-663a (ΔΔCt = 1.911, p = 9.75E-06) were confirmed in fluoxetine -treated SK-N-SH cells, while the up-regulated expression of miR-489 (ΔΔCt = 1.2, p = 0.007), miR-572 (ΔΔCt = 3.392, p = 3.81E-07) and miR-663a (ΔΔCt = 1.94, p = 1.77E-06) were confirmed in fluoxetine -treated SH-SY5Y cells (Fig 3). [score:11]
The expression of miR-572 has been found to be associated with cognitive dysfunction through down-regulation of one of its target, neuronal cell adhesion molecule 1 (NCAM1) [34]. [score:8]
Among the 13 miRNAs screened except miR-433, which was omitted from further analysis since the amplification was not proper in the cell lines studied, three miRNAs [miR-489 (p = 0.01 at 1μM), miR-572 (p = 0.009 at 1μM; p = 0.0004 at 5μM; p = 0.024 at 10μM); miR-663a (p = 0.032 at 5μM; p = 0.058 at 10μM)] were up-regulated in fluoxetine -treated (1-, 5- and 10-μM) SK-N-SH cells, while four miRNAs [miR-320a (p = 0.004 at 10μM), miR-489 (p = 0.037 at 10μM), miR-572 (p = 0.0002 at 5μM; p = 0.0004 at 10μM); miR-663a (p = 0.006 at 10μM)] were up-regulated in fluoxetine -treated SH-SY5Y cells compared to corresponding DMSO -treated control cells (Fig 2). [score:6]
The essential finding emerged from the current study was that fluoxetine (1–10 μM) up-regulated the expression of miR-572 and miR-663a consistently in two neuroblastoma cell lines SK-N-SH and SH-SY5Y. [score:6]
In addition to miR-572 and miR-663a, the expression of miR-489 was up-regulated in fluoxetine -treated SH-SY5Y cells. [score:6]
Yu et al (2015) have shown that increased miR-572 expression may lead to reduced downstream NCAM1 expression and loss of neuronal protection in patients with postoperative cognitive dysfunction [34]. [score:5]
Up-regulated expression of miRNAs (miR-320a, miR-489, miR-572 and miR-663a) in (a) SK-N-SH cells and (b) SH-SY5Y cells treated with various concentrations of fluoxetine compared to DMSO -treated control cells. [score:5]
Up-regulated expression of miR-572 and miR-663a in 10 μM fluoxetine -treated (a) SK-N-SH cells and (b) SH-SY5Y cells compared to DMSO -treated control cells. [score:5]
miR-489, miR-572 and miR-663a were consistently up-regulated in fluoxetine -treated SK-N-SH and SH-SY5Y cells. [score:4]
The expression of miR-320, miR-489, miR-572 and miR-663a were further compared between 10 μM fluoxetine (6 wells each) treated SK-N-SH and SH-SY5Y cells and their control cells. [score:2]
Confirmation qPCR experimental data with four miRNAs (miR-320, miR-489, miR-572 and miR-663a) of SH-SY5Y cells with 10-μM Fluoxetine and equal concentration of DMSO control. [score:1]
miR-572 has been implicated in the pathogenesis of several neurological disorders such as ASD [20, 24], schizophrenia [32] and multiple sclerosis [33]. [score:1]
Confirmation qPCR experimental data with four miRNAs (miR-320, miR-489, miR-572 and miR-663a) of SK-N-SH cells with 10-μM Fluoxetine and equal concentration of DMSO control. [score:1]
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4
[+] score: 40
MiR-151a-3p, miR-181b-5p, miR-320a, miR-328, miR-433, miR-489, miR-572 and miR-663a were downregulated, while miR-101-3p, miR-106b-5p, miR-19b-3p, miR-195-5p, miR-130a-3p and miR-27a-3p were upregulated. [score:7]
miR-151a-3p, miR-181b-5p, miR-320a, miR-328, miR-433, miR-489, miR-572 and miR-663a were downregulated while miR-101-3p, miR-106b-5p, miR-19b-3p, miR-195-5p, miR-130a-3p and miR-27a-3p were upregulated. [score:7]
miR-151a-3p (ΔΔCt = -2.01, P = 8.29E-06), MiR-181b-5p (ΔΔCt = -3.39, P = 1.04E-10), miR-320a (ΔΔCt = -2.47, P = 5.02E-12), miR-328 (ΔΔCt = -2.28, P = 4.33E-06), miR-433 (ΔΔCt = -2.33, P = 0.0001), miR-489 (ΔΔCt = -2.10, P = 1.25E-06), miR-572 (ΔΔCt = -2.47, P = 2.66E-08) and miR-663a (ΔΔCt = -2.06, P = 0.00002) were downregulated, while miR-101-3p (ΔΔCt = 1.43, P = 0.003), miR-106b-5p (ΔΔCt = 1.30, P = 0.008), miR-130a-3p (ΔΔCt = 2.35, P = 1.89E-09), miR-195-5p (ΔΔCt = 1.43, P = 0.0016) and miR-19b-3p (ΔΔCt = 1.87, P = 6.88E-09) were upregulated in the ASD individuals. [score:7]
MiR-151a-3p, miR-181b-5p, miR-320a, miR-328, miR-433, miR-489, miR-572, and miR-663a were downregulated, while miR-101-3p, miR-106b-5p, miR-130a-3p, miR-195-5p, and miR-19b-3p were upregulated. [score:7]
The differentially expressed miRNAs in this study, which included miR-101, miR-106b, miR-130a, miR-151a, miR181b, miR-328, miR-433, miR-489 and miR-572, were previously reported to have altered expression in schizophrenia [31- 35], supporting the contention that ASD and schizophrenia share common neurobiological features [36]. [score:5]
Collectively, these results predicted several neurologically relevant canonical pathways for the target genes of the five miRNAs (miR-130a-3p, miR-19b-3p, miR-320a, miR181b-5p, and miR-572) that showed a good discriminative power in ROC analysis. [score:3]
High values for sensitivity, specificity and area under the curve (AUC) were observed for five miRNAs: miR-181b-5p, miR-320a, miR-572, miR-130a-3p and miR-19b-3p (see Additional file 6). [score:1]
High values for sensitivity, specificity and the area under the curve (AUC) were observed for five miRNAs: miR-181b-5p, miR-320a, miR-572, miR-130a-3p and miR-19b-3p (see Additional file 6). [score:1]
The Ct values of nine miRNAs (miR-101-3p, miR-106b-5p, miR-151a-3p, miR-195-5p, miR-19b-3p, miR-27a-3p, miR-320a, miR-328, and miR-489) were in the range of 25–30, while the remaining five miRNAs (miR-130a-3p, miR-181b-5p, miR-433, miR-572, and miR-663a) had Ct values in the range of 30 to 35. [score:1]
No specific pathways were observed for miR-572. [score:1]
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5
[+] score: 24
Interestingly, the expression of these miRNAs were also enhanced in cells infected with West Nile virus (WNV), but upregulation for miR-3687 and miR-572 were more pronounced and significantly upregulated in JEV infected cells (Fig. 3K). [score:9]
Consistent upregulation across 48 h pi was observed with miR-3648, miR-3687, miR-129-5p, miR-572, and two-way ANOVA confirmed that infection is the main factor in miRNAs deregulation as their expression increased along with increasing viral load (P < 0.001) (Fig. 3A–D). [score:7]
Although upregulation pattern of seven miRNAs was noted in cells infected with WNV, enhancement is more pronounced in JEV infected cells especially for miR-3646, miR-4470 (Fig. 6C), miR-572 and miR-3687, suggesting their possible JEV specific role during infection. [score:4]
As shown in Fig. 3J, the expression of miR-3648, miR-3687, miR-129-5p, miR-572, increased with increased MOI used for initial infection in human microglial cells. [score:3]
The results of qPCR analysis of (A) miR-3648, (B) miR-3687 (C) miR-572, (D) miR-129-5p, (E) miR-197-3p, (F) miR-145-5p, (G) miR-374b-5p, (H) miR-26b-5p, (I) miR-149-5p, at three different time points are presented. [score:1]
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6
[+] score: 23
Figure 2(A) Expression of miR-659-3p, (B) miR-572, (C) CNOT1, GSTE1 and KIF4A and (D) inverse correlation between miR-659-3p and CNOT1 expression in HTLA-230 and SH-SY5Y cells treated with miR-659-3p mimic and inhibitorResults of RT-qPCR analysis from two independent experiments are reported as Log [10] of relative expression respect to that occurring in cells treated with irrelevant miRNA mimic and inhibitor. [score:11]
As shown in Figure 2A, treatment with miR-659-3p mimic and inhibitor respectively increased and decreased miR-659-3p expression as compared to cells treated with the irrelevant mimic and inhibitor, whereas the expression of the unrelated miR-572 was unaffected (Figure 2B). [score:8]
As control of specificity, each sample was tested in triplicates for miR-572 expression using the specific TaqMan [©] assay. [score:2]
To validate the differential expression of the selected 20 miRNAs, reverse-transcribed and pre-amplified miRNA fractions from 10 additional BM-infiltrating and 10 primary tumors were amplified in a 96 well plate in triplicate using the specific TaqMan [©] human microRNA assays (hsa-miR-324-3p, catalog #002161; hsa-miR-516-3p, catalog #001149; hsa-miR-628-5p, catalog #002433; hsa-miR-659-3p, catalog #001514; hsa-miR-10b, catalog #002218; hsa-miR-128, catalog #002216; mmu-miR-137, catalog #01129; mmu-miR-140, catalog #001187; hsa-miR-16, catalog #000391, hsa-miR-191, catalog #002299; hsa-miR-301, catalog #000528; hsa-miR-361-3p, catalog #002116; hsa-miR-365, catalog #001020; hsa-miR-548d-3p, catalog #001605; hsa-miR-572, catalog #001614; hsa-miR-576-5p, catalog #002350, hsa-miR-616, catalog #001589; hsa-miR-628-3p, catalog #002434; hsa-miR-873, catalog #002356; hsa-miR-98, catalog #000577; U6 snRNA, catalog #001973, Life Technologies). [score:2]
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7
[+] score: 22
Other miRNAs from this paper: hsa-mir-93
By doing so, we obtained the p21 response after genotoxic stress in four scenarios: (1) endogenous miRNA expression (Control); (2) overexpression of miR-572; (3) overexpression of miR-93; and (4) both miRNAs moderately overexpressed. [score:9]
The individual overexpression of miR-572 or miR-93 led to the reduction of the upregulation of p21 response after genotoxic stress induction. [score:6]
In Figure 3(a), the network module contains an incoherent FFL composed by AF2 α, miR-93 and p21, and a cascaded regulation in which p21 is repressed by FOXF2 via miR-572; in Figure 3(b), the same cascaded regulation together with a coherent FFL composed of TP53, MYC, miR-93 and p21 forms another regulatory module of p21. [score:4]
To experimentally validate the capability of our mo del to predict the relative p21 concentrations regulated by cooperative miRNAs, we selected miR-572 and miR-93 as a case study. [score:2]
To do so, two network modules including both miR-93 and miR-572, and their TFs were exemplified. [score:1]
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8
[+] score: 8
MiR-572 prompted cell proliferation of human ovarian cancer cells by suppressing PPP2R2C expression. [score:4]
Nineteen of the downregulated miRNAs in chronic patients were found to be associated with carcinogenesis in various organs and tissues, such as miR-1207 [40], miR-3162-5p [41, 42], miR-3196 [43, 44], miR-371b-5p [45], miR-574-5p [46, 47], miR-1225-5p [48], miR-4485 [49], miR-572 [50], miR-4299 [51], miR-3679-5p [52], miR-3940-5p [53], miR-638 [54, 55], miR-1202 [56], miR-5787 [57], miR-1973 [58], miR-4532 [59], miR-1275 [60], miR-4728-5p [61], and miR-1915-3p [62]. [score:4]
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[+] score: 7
While miR-1290 and miR-572 were found to be upregulated, miR-125a-3p, miR-134, miR-584-5p, miR-663a, and miR-513a-5p were determined to be downregulated in various types of cancer [48– 64]. [score:7]
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[+] score: 7
In human melanoma cells, miR-93 and miR-572 displayed cooperative inhibitory effects on the expression of cyclin -dependent kinase inhibitor p21 [20]. [score:7]
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[+] score: 6
To demonstrate a proof of principle we repeated the described protocol for the RNA triplex composed of miRNA-93:: CDKN1A::miRNA-572 for which we previously validated the synergistic effect the two miRNAs show in the repression of their mutual target (13). [score:3]
In our own previous work we have analyzed this phenomenon and validated it in human SK-Mel-147 melanoma cells for the case of p21 which is regulated by miRNA-93 and miR-572 (3). [score:2]
Our simulations show that the duplexes miRNA-572:: CDKN1A and miRNA-93:: CDKN1A are stable for 42 and 301 ps in the production run, while in the RNA triplex the stability times of miRNA-572 and miRNA-93 increase to 126 and 473 ps, respectively. [score:1]
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[+] score: 5
For instance, miR-10b-5p, miR-205-5p and miR-214-3p are shown to be expressed in mouse and human ovaries [28, 29]; the expression of miR-572, miR-214-3p and miR-205-5p have been detected in human endometrium [30– 32]. [score:5]
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13
[+] score: 4
Other miRNAs are predicted to bind SOCS1, including mir-150 (172), mir-221 (173), mir-572 (174), and mir-19a (175); upregulation of these miRNAs correlates with increased inflammation. [score:4]
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[+] score: 4
Among the top ten fold changed miRNAs (Supplementary Table 1), half of them (hsa-miR-371b-5p, hsa-miR-663a, hsa-miR-1225-5p, hsa-miR-1202, and hsa-miR-572) were closely linked to the occurrence and development of tumors and might play vital roles as oncogenes or tumor suppressor genes [28– 31]. [score:4]
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[+] score: 4
Intriguingly, the finding of another peripheral study using a cohort of preterm infants and adults [35] showed that six (hsa-miR-34a, hsa-miR-449a, hsa-miR-564, hsa-miR-432, hsa-miR-548d and hsa-miR-572) of the seven schizophrenia -associated miRNAs were consistently expressed from infancy to adulthood. [score:3]
We previously identified a seven-miRNA (hsa-miR-34a, miR-449a, miR-564, miR-432, miR-548d, miR-572 and miR-652) signature as a potential biomarker for schizophrenia. [score:1]
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[+] score: 4
For H1N1 infected cells, at 18 and 24-hour post-infection, miR-188-5p, miR-1260, miR-1274a, miR-1274b, miR141, miR183*, miR-18b, miR-19a, miR21*, miR-301a, miR-572, miR-720, and miR-939 were found to be up-regulated (>1.5-fold, p<0.05) (Table 1). [score:4]
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[+] score: 3
Similarly, by comparing expression profiles of miRNAs in the plasma of patients with prediabetes and newly diagnosed T2DM, Yan et al. demonstrated plasma miR-1249, miR-320b, and miR-572 levels as potential biomarkers for early diagnosis of T2DM [65]. [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-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-25, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-198, hsa-mir-199a-1, hsa-mir-148a, 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-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-27b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-142, hsa-mir-145, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-146a, hsa-mir-150, hsa-mir-186, hsa-mir-188, hsa-mir-193a, hsa-mir-194-1, hsa-mir-320a, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-362, hsa-mir-369, hsa-mir-375, hsa-mir-378a, hsa-mir-382, hsa-mir-340, hsa-mir-328, hsa-mir-342, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-339, hsa-mir-335, hsa-mir-345, hsa-mir-196b, hsa-mir-424, hsa-mir-425, hsa-mir-20b, hsa-mir-451a, hsa-mir-409, hsa-mir-484, hsa-mir-486-1, hsa-mir-487a, hsa-mir-511, hsa-mir-146b, hsa-mir-496, hsa-mir-181d, hsa-mir-523, hsa-mir-518d, hsa-mir-499a, hsa-mir-501, hsa-mir-532, hsa-mir-487b, hsa-mir-551a, hsa-mir-92b, hsa-mir-580, hsa-mir-550a-1, hsa-mir-550a-2, hsa-mir-590, hsa-mir-599, hsa-mir-612, hsa-mir-624, hsa-mir-625, hsa-mir-627, hsa-mir-629, hsa-mir-33b, hsa-mir-633, hsa-mir-638, hsa-mir-644a, hsa-mir-650, hsa-mir-548d-1, hsa-mir-449b, hsa-mir-550a-3, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-454, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-708, hsa-mir-216b, hsa-mir-1290, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-3151, hsa-mir-320e, hsa-mir-378c, hsa-mir-550b-1, hsa-mir-550b-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-219b, hsa-mir-203b, hsa-mir-451b, hsa-mir-499b, hsa-mir-378j, hsa-mir-486-2
microRNA analysis from different studies showed that expression of miR-10a, miR-134, miR-214, miR-221, miR-128b, miR-484, miR-572, miR-580, miR-624 and miR-627 was significantly correlated with a favorable clinical outcome [61, 65, 67]. [score:3]
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[+] score: 2
Briefly, miRNA was reverse transcribed using sequence specific stem-loop primers (invitrogen) to the following miRNAs: hsa-miR-125b, hsa-miR-145, hsa-miR-153, hsa-miR-210, hsa-miR-143, hsa-miR-100, hsa-miR-363, hsa-miR-451, hsa-miR-572 and hsa-miR-508-5p, based on microarray analysis and their predicted target genes. [score:2]
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Other miRNAs from this paper: hsa-let-7a-2, hsa-let-7c, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-2, hsa-mir-100, hsa-mir-29b-2, mmu-let-7i, mmu-mir-99b, mmu-mir-125a, mmu-mir-130a, mmu-mir-142a, mmu-mir-144, mmu-mir-155, mmu-mir-183, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-148a, mmu-mir-143, hsa-mir-181c, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-298, mmu-mir-34b, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-130a, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-125a, mmu-mir-148a, mmu-mir-196a-1, mmu-let-7a-2, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-mir-15a, mmu-mir-16-1, mmu-mir-21a, mmu-mir-22, mmu-mir-23a, mmu-mir-24-2, rno-mir-148b, mmu-mir-148b, hsa-mir-200c, hsa-mir-155, mmu-mir-100, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181c, hsa-mir-34b, hsa-mir-99b, hsa-mir-374a, hsa-mir-148b, rno-let-7a-2, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7i, rno-mir-21, rno-mir-22, rno-mir-23a, rno-mir-24-2, rno-mir-29b-2, rno-mir-34b, rno-mir-99b, rno-mir-100, rno-mir-124-1, rno-mir-124-2, rno-mir-125a, rno-mir-130a, rno-mir-142, rno-mir-143, rno-mir-144, rno-mir-181c, rno-mir-183, rno-mir-199a, rno-mir-200c, rno-mir-200b, rno-mir-181a-1, rno-mir-298, hsa-mir-193b, hsa-mir-497, hsa-mir-568, hsa-mir-596, hsa-mir-612, rno-mir-664-1, rno-mir-664-2, rno-mir-497, mmu-mir-374b, mmu-mir-497a, mmu-mir-193b, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-568, hsa-mir-298, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, hsa-mir-664a, mmu-mir-664, rno-mir-568, hsa-mir-664b, mmu-mir-21b, mmu-mir-21c, rno-mir-155, mmu-mir-142b, mmu-mir-497b, rno-mir-148a, rno-mir-15a, rno-mir-193b
Genomic coordinates are provided in Additional file 1. Figure 7 Transcription features mapped in the flanking regions surrounding hsa-mir-550-2. Figure 8 Graphical display of transcription features mapped in the flanking regions surrounding miRNAs of Group IV; (a) hsa-mir-572 and (b) mmu-mir-715. [score:1]
Genomic coordinates are provided in Additional file 1. Figure 7 Transcription features mapped in the flanking regions surrounding hsa-mir-550-2. Figure 8 Graphical display of transcription features mapped in the flanking regions surrounding miRNAs of Group IV; (a) hsa-mir-572 and (b) mmu-mir-715. [score:1]
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Indeed, some miRNAs became undetectable (miR-1274B, miR-572, and miR-766), while others appeared de novo in cells (miR-140-5p, miR-222*, miR-376c, miR-411, and miR-146a) and their SNs (miR-146a, miR-146b, miR-19a, miR-223*, miR-425, and miR-9*) upon MCM -induced inflammation (Figure  2). [score:1]
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From these a seven-miRNA signature (miR-34a, miR-449a, miR-564, miR-432, miR-548d, miR-572 and miR-652) was identified using stepwise logistic regression analysis, with a fold-change ranging from −1.4 to 2.5 (Table 1 ). [score:1]
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[+] score: 1
Mononuclear leukocyte -based miR profiling identified seven miRs, that is, miR-34a, miR- 449a, miR-564, miR-432, miR-548d, miR-572, miR-652 and had a high discriminating accuracy for schizophrenia. [score:1]
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Interestingly, more positively correlated microRNA-mRNA pairs than negatively correlated pairs were observed for all microRNAs with the exception of nine, miR-181B2, miR-582, miR-497, miR-559, miR-561, miR-101-1, miR-187, miR-572 and miR-301A (Figure 5). [score:1]
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It was clearly demonstrated by ROC analysis that the 5-miRNA -based panels (miR-193a-3p, miR-362, miR-572, miR-425-5p, and miR-543) had a high sensitivity and specificity in the discrimination of patients with early-stage RCC from healthy controls [54]. [score:1]
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