MiR-495 is a Predictive Biomarker that Downregulates GFI1 Expression in Medulloblastoma

Yun, Zhiyuan; Zhao, Tianshu; Liu, Xian; Ma, Xueling

doi:10.1159/000430308

Cited by 23 publications

(15 citation statements)

References 35 publications

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“…Multivariate analysis also demonstrates miR-495 as an independent predictor of the overall survival of patients with medulloblastoma (35). miR-495 is weakly expressed in prostate cancer and associated with prostate-specific antigen levels, lymph node invasion and Gleason scores (36).…”

Section: Discussionmentioning

confidence: 89%

MicroRNA‑495 suppresses cell proliferation and invasion of hepatocellular carcinoma by directly targeting insulin‑like growth factor receptor‑1

Zhuang

Wang

et al. 2017

Exp Ther Med

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Abstract. Hepatocellular carcinoma (HCC) is the fifth most common malignancy and second-most frequent cause of cancer-associated deaths worldwide. Previously, increasing studies report that microRNAs (miRNAs/miRs) are abnormally expressed in various types of human cancers and may participate in the tumourigenesis and tumour development of HCC. miRNA-based targeted therapy is effective against different molecular targets and may increase the sensitisation of cancer cells to therapy by several folds. Therefore, further validation of potentially important miRNAs involved in HCC initiation and progression may provide valuable insights into the treatment of patients with HCC. miR-495 is abnormally expressed in multiple types of human cancers. However, the expression level and roles of miR-495 in HCC have yet to be completely elucidated. In the present study, miR-495 expression was frequently downregulated in HCC tissues and cell lines, and miR-495 expression levels were significantly correlated with tumour size, tumor-node-metastasis (TNM) stage and lymph node metastasis in patients with HCC. Functional assays revealed that miR-495 overexpression inhibited cell proliferation and invasion in HCC. Insulin-like growth factor receptor-1 (IGF1R) was identified as a direct target gene of miR-495 in HCC. IGF1R was upregulated in HCC tissues and negatively correlated with miR-495 expression level. The upregulation of IGF1R rescued the miR-495-induced tumour-suppressive roles in HCC cell proliferation and invasion, and the restored miR-495 expression inactivated the protein kinase B and extracellular regulated protein kinase signalling pathways in HCC. These results provide novel insights into the molecular mechanism underlying HCC progression, and suggest that miR-495 may be investigated as a novel therapeutic target for patients with this disease.

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Section: Discussionmentioning

confidence: 89%

MicroRNA‑495 suppresses cell proliferation and invasion of hepatocellular carcinoma by directly targeting insulin‑like growth factor receptor‑1

Zhuang

Wang

et al. 2017

Exp Ther Med

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“…Downregulation of miR-495 is frequently observed in various types of human cancer (21)(22)(23)(24). For example, miR-495 is downregulated in medulloblastoma tissues and cell lines; patients with medulloblastoma and decreased expression levels of miR-495 exhibit poorer prognosis compared with those expressing higher miR-495 levels (21). Furthermore, miR-495 has been reported as an independent predictor of overall survival in patients with medulloblastoma (21).…”

Section: Discussionmentioning

confidence: 99%

“…For example, miR-495 is downregulated in medulloblastoma tissues and cell lines; patients with medulloblastoma and decreased expression levels of miR-495 exhibit poorer prognosis compared with those expressing higher miR-495 levels (21). Furthermore, miR-495 has been reported as an independent predictor of overall survival in patients with medulloblastoma (21). In esophageal squamous cell carcinoma, the expression levels of miR-495 were reported to be reduced in tumor tissues and significantly associated with lymph node metastasis, invasion and tumor, node and metastasis (TNM) stage (22).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑495 targets Notch1 to prohibit cell proliferation and invasion in oral squamous cell carcinoma

Wang

Yang

et al. 2018

Mol Med Report

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MicroRNAs (miRNAs) are associated with the initiation and progression of oral squamous cell carcinoma (OSCC) by regulating a variety of cancer-associated behaviors. Fully understanding the regulatory mechanism of miRNAs in the pathogenesis of OSCC may provide novel promising approaches for the identification of prognostic biomarkers and therapeutic targets for this particular malignancy. In the present study, reverse transcription-quantitative polymerase chain reaction analysis was performed to detect miRNA (miR)-495 expression in OSCC tissues and cell lines. The effects of miR-495 on the proliferation and invasion of OSCC cells were determined using Cell Counting Kit-8 and Matrigel invasion assays, respectively. The mechanisms underlying the action of miR-495 in OSCC cells were also investigated. Results from the present study revealed that miR-495 expression was downregulated in OSCC tissues and cell lines compare with in adjacent normal tissues and human oral keratinocytes, respectively. Exogenous expression of miR-495 restricted cell proliferation and invasion of OSCC cells in vitro. Notch1 was identified as a direct functional target of miR-495 in OSCC. Furthermore, Notch1 knockdown exhibited inhibitory effects, similar to those induced by miR-495 overexpression in OSCC cells. Restoration of Notch1 expression rescued the suppressive effects of miR-495 on OSCC cell proliferation and invasion. These findings suggested an important role for miR-495 in the regulation of OSCC cell growth and metastasis, at least partly by directly targeting Notch1. In addition, the findings of the present study revealed the potential of miR-495 as a novel therapeutic target for the treatment of patients with OSCC.

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“…miR‐495 is involved in type II diabetes in mice . In addition, miR‐495 participates in the pathogenesis of cancer . In differentiation, miR‐495 inhibits chondrogenic differentiation in human mesenchymal stem cells by targeting Sox9 .…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐495 regulates starvation‐induced autophagy by targeting ATG3

Yang

Hou

et al. 2016

FEBS Letters

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The functions of some essential autophagy genes are regulated by microRNAs. However, an ATG3-modulating microRNA has never been reported. Here we show that the transcription of miR-495 negatively correlates with the translation of ATG3 under nutrient-deprived or rapamycin-treated conditions. miR-495 targets ATG3 and regulates its protein levels under starvation conditions. miR-495 also inhibits starvation-induced autophagy by decreasing the number of autophagosomes and by preventing LC3-I-to-LC3-II transition and P62 degradation. These processes are reversed by the overexpression of an endogenous miR-495 inhibitor. Re-expression of Atg3 without miR-495 response elements restores miR-495-inhibited autophagy. miR-495 sustains cell viability under starvation conditions but has no effect under hypoxia. Moreover, miR-495 inhibits etoposide-induced cell death. In conclusion, miR-495 is involved in starvation-induced autophagy by regulating Atg3.

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MiR-495 is a Predictive Biomarker that Downregulates GFI1 Expression in Medulloblastoma

Cited by 23 publications

References 35 publications

MicroRNA‑495 suppresses cell proliferation and invasion of hepatocellular carcinoma by directly targeting insulin‑like growth factor receptor‑1

MicroRNA‑495 suppresses cell proliferation and invasion of hepatocellular carcinoma by directly targeting insulin‑like growth factor receptor‑1

MicroRNA‑495 targets Notch1 to prohibit cell proliferation and invasion in oral squamous cell carcinoma

MicroRNA‐495 regulates starvation‐induced autophagy by targeting ATG3

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