miR-9 Acts as an OncomiR in Prostate Cancer through Multiple Pathways That Drive Tumour Progression and Metastasis

Seashols‐Williams, Sarah; Budd, William T.; Clark, Gene C; Wu, Qianni; Daniel, Rosy; Dragoescu, Ema; Zehner, Zendra E.

doi:10.1371/journal.pone.0159601

Cited by 57 publications

(53 citation statements)

References 54 publications

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“…Given the importance of inflammation in the development of HCC, the identification of one of the SOCS family members as a tumor suppressor for liver cancer is particularly relevant. SOCS5 was found to be downregulated in normal endothelial cells showing a miR-9-mediated enhanced endothelial cell migration and was validated as a miR-9 target, 26,39 suggesting its potential role as a tumor suppressor. In addition, the Drosophila orthologue of SOCS5, SOCS36E, behaves as a tumor suppressor in EGFR-driven tumor models.…”

Section: Discussionmentioning

confidence: 97%

A novel SOCS5/miR‐18/miR‐25 axis promotes tumorigenesis in liver cancer

Sánchez-Mejías

Kwon

Chew

et al. 2018

Intl Journal of Cancer

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The role of miRNAs with tumor suppressive activity in liver cancer has been well studied. However, little is known about potential oncomiRs in HCC. In our study, we conducted a systematic evaluation of candidate oncomiRs and found that upregulation of miR-18a and miR-25 in HCC was associated with poor patient survival and promoted proliferation in HCC cell lines. These two miRNAs belong to the polycistronic paralogous miR-17-92 and miR-25-106b clusters respectively. Although the members of both clusters are often upregulated in HCC, the contribution of individual miRNAs in these clusters to HCC tumorigenesis is not fully understood. We validated SOCS5 as a bona fide target of both miRNAs, and established, for the first time, the tumor suppressive role of SOCS5 in liver cancer. We further investigated the mechanism by which SOCS5 contributes to tumorigenesis, demonstrated that this SOCS5/miR-18a/miR-25 axis regulates the tumor suppressor TSC1 and downstream mTOR signaling, and highlighted the potential therapeutic use of miR-18a and miR-25 inhibition in restoring SOCS5 levels in HCC.

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Section: Discussionmentioning

confidence: 97%

A novel SOCS5/miR‐18/miR‐25 axis promotes tumorigenesis in liver cancer

Sánchez-Mejías

Kwon

Chew

et al. 2018

Intl Journal of Cancer

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“…MiR‐9 has been demonstrated to be involved in tumorigenesis and development . A recent study has reported that miR‐9 is up‐regulated and acts as a pro‐metastatic miRNA in breast cancer cells.…”

Section: Discussionmentioning

confidence: 99%

“…MiR‐9 has various expression patterns in diverse human cancers, and it plays different roles in different cancer types . Xu et al .…”

Section: Introductionmentioning

confidence: 99%

MiR‐9 is involved in TGF‐β1‐induced lung cancer cell invasion and adhesion by targeting SOX7

Han

Wang

Ding

et al. 2017

J Cellular Molecular Medi

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MicroRNA (miR)‐9 plays different roles in different cancer types. Here, we investigated the role of miR‐9 in non‐small‐cell lung cancer (NSCLC) cell invasion and adhesion in vitro and explored whether miR‐9 was involved in transforming growth factor‐beta 1 (TGF‐β1)‐induced NSCLC cell invasion and adhesion by targeting SOX7. The expression of miR‐9 and SOX7 in human NSCLC tissues and cell lines was examined by reverse transcription‐quantitative polymerase chain reaction. Gain‐of‐function and loss‐of‐function experiments were performed on A549 and HCC827 cells to investigate the effect of miR‐9 and SOX7 on NSCLC cell invasion and adhesion in the presence or absence of TGF‐β1. Transwell–Matrigel assay and cell adhesion assay were used to examine cell invasion and adhesion abilities. Luciferase reporter assay was performed to determine whether SOX7 was a direct target of miR‐9. We found miR‐9 was up‐regulated and SOX7 was down‐regulated in human NSCLC tissues and cell lines. Moreover, SOX7 expression was negatively correlated with miR‐9 expression. miR‐9 knockdown or SOX7 overexpression could suppress TGF‐β1‐induced NSCLC cell invasion and adhesion. miR‐9 directly targets the 3′ untranslated region of SOX7, and SOX7 protein expression was down‐regulated by miR‐9. TGF‐β1 induced miR‐9 expression in NSCLC cells. miR‐9 up‐regulation led to enhanced NSCLC cell invasion and adhesion; however, these effects could be attenuated by SOX7 overexpression. We concluded that miR‐9 expression was negatively correlated with SOX7 expression in human NSCLC. miR‐9 was up‐regulated by TGF‐β1 and contributed to TGF‐β1‐induced NSCLC cell invasion and adhesion by directly targeting SOX7.

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“…miRNAs regulate gene expression by base-pairing with the 3' untranslated regions (3'UTRs) of their target genes, resulting in translational suppression or mRNA degradation, and ultimately controlling the protein expression of target genes (7). It has previously been demonstrated that miRNAs are important in various biological processes, including cell proliferation, cell cycle, differentiation and metastasis (8)(9)(10). miRNAs have been reported to be downregulated or upregulated in a variety of human malignancies (11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-320 targets mitogen-activated protein kinase 1 to inhibit cell proliferation and invasion in epithelial ovarian cancer

Zhang

et al. 2017

Molecular Medicine Reports

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Ovarian cancer is the second most frequently occurring cancer and the most fatal gynecological malignancy of all gynecological cancers worldwide. MicroRNAs (miR) have been reported to be downregulated or upregulated in a variety of human malignancies, and involved in the formation and progression of the majority of human cancers, including epithelial ovarian cancer (EOC). miR‑320 has been identified as a tumor suppressor in multiple human cancers. However, the expression levels, biological role and underlying mechanisms of miR‑320 in EOC remain to be elucidated. In the present study, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was performed to detect miR‑320 expression in EOC tissues and cell lines. Following transfection with miR‑320 mimics, Cell Counting Kit 8 and cell invasion assays were utilized to investigate the effects of miR‑320 on EOC cell proliferation and invasion. Bioinformatic analysis, luciferase reporter assay, RT‑qPCR and western blotting were used to explore the underlying mechanism of how miR‑320 affects cell proliferation and invasion in EOC. Mitogen‑activated protein kinase (MAPK) 1 expression and its association with the miR‑320 expression level was examined in EOC tissues. The role of MAPK1 in EOC cells was additionally evaluated by using a loss‑of‑function assay. The results demonstrated that miR‑320 was markedly downregulated in EOC tissues and cell lines. A decreased miR‑320 expression was significantly correlated with the Federation of Gynecology and Obstetrics stage and lymph node metastasis of EOC patients. Additionally, reintroduction of miR‑320 expression suppressed cell proliferation and invasion in EOC. Furthermore, it was verified that MAPK1 is a direct target gene of miR‑320 in EOC. MAPK1 expression was markedly upregulated in EOC tissues and inversely correlated with miR‑320 expression. Furthermore, silencing of MAPK1 by RNA interference inhibited cell proliferation and invasion of EOC cells. Overall, the present study demonstrated that miR‑320 may act as a useful diagnostic and therapeutic target in the treatment of EOC.

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miR-9 Acts as an OncomiR in Prostate Cancer through Multiple Pathways That Drive Tumour Progression and Metastasis

Cited by 57 publications

References 54 publications

A novel SOCS5/miR‐18/miR‐25 axis promotes tumorigenesis in liver cancer

A novel SOCS5/miR‐18/miR‐25 axis promotes tumorigenesis in liver cancer

MiR‐9 is involved in TGF‐β1‐induced lung cancer cell invasion and adhesion by targeting SOX7

MicroRNA-320 targets mitogen-activated protein kinase 1 to inhibit cell proliferation and invasion in epithelial ovarian cancer

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