Dysregulation of mi<scp>R</scp>‐31 and mi<scp>R</scp>‐375 expression is associated with clinical outcomes in oral carcinoma

Siow, M Y; Ng, LP Karen; Chong, VK Vincent; Marhazlinda, Jamaludin; Abraham, Mannil Thomas; Rahman, Zulkanain Abdul; Tg, Kallarakkal; Yang, Yi‐Hsin; Cheong, S C; Rb, Zain

doi:10.1111/odi.12118

Cited by 65 publications

(54 citation statements)

References 32 publications

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“…These results indicated that reduced expression levels of miR-375 may induce more aggressive tumor behavior during oral cancer progression. These results are similar to those reported by Siow et al (18), who demonstrated that low miR-375 expression levels were significantly associated with late-stage disease, larger tumor size and a non-cohesive pattern of invasion in OSCC.…”

Section: Discussionsupporting

confidence: 91%

MicroRNA-375 inhibits oral squamous cell carcinoma cell migration and invasion by targeting platelet-derived growth factor-A

Cao

Cheng

Zhang

et al. 2016

Molecular Medicine Reports

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Abstract. serves an important role in cancer development and growth. However, little is known about the role of miR-375 in the regulation of oral squamous cell carcinoma (OSCC) metastasis and invasion. The present study measured the expression levels of miR-375 in Tca8113, UM2, UM1 and CAL-27 cell lines, using reverse transcription-quantitative polymerase chain reaction. The results demonstrated that miR-375 expression levels were significantly reduced in UM1 and CAL-27 (highly metastatic) compared with Tca8113 and UM2 (less aggressive) OSCC cell lines. Furthermore, it was revealed that overexpression of miR-375 suppressed the migration and invasion of UM1 cells. Based on a luciferase reporter assay, platelet-derived growth factor-A (PDGF-A) was identified as a direct target gene of miR-375. Additionally, overexpression of PDGF-A significantly reversed the effect of miR-375 on cell migration and invasion in UM1 cells. These data demonstrated that miR-375 suppressed OSCC cell migration and invasion by targeting PDGF-A, which may be a potential therapeutic target for the treatment of OSCC.

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Section: Discussionsupporting

confidence: 91%

MicroRNA-375 inhibits oral squamous cell carcinoma cell migration and invasion by targeting platelet-derived growth factor-A

Cao

Cheng

Zhang

et al. 2016

Molecular Medicine Reports

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“…Previous studies showed that miR-31 was emerging as an important regulator in carcinoma [15][16][17][18]. In the present study, we report that miR-31, a differentially expressed miRNA during fibrogenesis, significantly promotes HSC activation and migration.…”

Section: Introductionmentioning

confidence: 56%

The role of the miR-31/FIH1 pathway in TGF-β-induced liver fibrosis

Chen

Liu

et al. 2015

Clinical Science

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The miRNAs are small, non-coding RNAs that regulate various biological processes, including liver fibrosis. Hepatic stellate cells (HSCs) play a central role in the pathogenesis of liver fibrosis. By microarray profiling and real-time PCR, we noted that miR-31 expression in HSCs from rats, mice and humans was significantly increased during HSC activation in culture. Overall, miR-31 expression levels were unchanged in the whole-liver RNA extracts from fibrotic rat and human samples. Nevertheless, we found that miR-31 was particularly up-regulated in HSCs but not in hepatocytes during fibrogenesis. Thus, we hypothesized that miR-31 may mediate liver fibrosis. In the present study, we found that inhibition of miR-31 expression significantly inhibited HSC activation, whereas its over-expression obviously promoted HSC activation. Moreover, over-expression of miR-31 promoted HSC migration by enhancing matrix metalloproteinase (MMP)-2 expression whereas inhibition of miR-31 has an opposite effect. The biological function of miR-31 during HSC activation might be through targeting FIH1, a suppressor of hypoxia-inducible factor (HIF-1), because a knockdown of FIH1 by shRNA could mimic the effects of miR-31. In addition, primary rat HSCs were isolated and treated with different cytokines, such as transforming growth factor β (TGF-β), vascular endothelial growth factor and platelet-derived growth factor-BB, to evaluate upstream regulators of miR-31. We found that only TGF-β, a pivotal regulator in liver fibrosis, remarkably increased miR-31 expression in HSCs. And the effects of TGF-β on HSCs can be partially counteracted by inhibition of miR-31. In addition, chromatin immunoprecipitation experiments and the luciferase reporter assay demonstrated that Smad3, a major TGF-β-downstream transcription factor, stimulated the transcription activity of miR-31 by binding directly to miR-31's promoter. In conclusion, the miR-31/FIH1 pathway associates with liver fibrosis, perhaps by participation in the TGF-β/Smad3 signalling of HSCs.

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“…Deregulated miR-375 expression has been indicated in various cancer types including oral carcinoma [17], breast cancer [18], esophageal adenocarcinoma, lung cancer [19], glioma [20], gastric cancer [21], and hepatocellular carcinoma [22]. More recently, elevated miR-375 expression was found in gastric cancer, and miR-375 can desensitize cells to ionizing radiation and etoposide by targeting p53 [23].…”

Section: Discussionmentioning

confidence: 97%

MicroRNA-375 functions as a tumor suppressor in osteosarcoma by targeting PIK3CA

Shi

Chu

et al. 2015

Tumor Biol.

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Osteosarcoma has become one of the most common primary malignant bone tumors in childhood and adult. Numerous studies have demonstrated that aberrant microRNA (miRNA) expression is involved in human disease including cancer. To date, the potential miRNAs regulating osteosarcoma growth and progression are not fully identified yet. Herein, we showed that miR-375 was frequently downregulated in osteosarcoma tissue and cell lines compared to normal human colon tissues. Overexpression of miR-375 resulted in decreased expression of PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha) at both mRNA and protein levels. We found that miR-375 overexpression markedly suppressed cell proliferation in vitro. And inhibition of miR-375 promotes osteosarcoma growth. Mechanistic studies showed that PIK3CA was a potential target of miR-375 and it mediated reduction of PIK3CA resulted in suppression of PI3K/Akt pathway. Taken together, our results demonstrate that miR-375 functions as a growth-suppressive miRNA and plays an important role in inhibiting the tumorigenesis through targeting PIK3CA in osteosarcoma.

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Dysregulation of miR‐31 and miR‐375 expression is associated with clinical outcomes in oral carcinoma

Abstract: This study has identified 19 miRNAs significantly associated with OSCC, and expressions of miR-31 and miR-375 were significantly related with clinico-pathological parameters suggesting they could be important in driving oral tumourigenesis.

Cited by 65 publications

References 32 publications

MicroRNA-375 inhibits oral squamous cell carcinoma cell migration and invasion by targeting platelet-derived growth factor-A

MicroRNA-375 inhibits oral squamous cell carcinoma cell migration and invasion by targeting platelet-derived growth factor-A

The role of the miR-31/FIH1 pathway in TGF-β-induced liver fibrosis

MicroRNA-375 functions as a tumor suppressor in osteosarcoma by targeting PIK3CA

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