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MicroRNA?518b functions as a tumor suppressor in glioblastoma by targeting PDGFRB.

ABSTRACT: Glioblastoma (GBM) is the most common and aggressive type of primary human brain tumor in China. Dysregulated microRNA (miRNA/miR) expression has been hypothesized to serve a role in the tumorigenesis and progression of human GBM. To explore the potential mechanisms affecting GBM tumorigenesis, the function of miR?518b in regulating GBM cell proliferation and angiogenesis was examined in vitro by CCK?8 and tube formation assay and in vivo by xenograft assay. The present study demonstrated that the expression of miR?518b was downregulated in GBM tissues and in GBM cell lines (U87 and U251). In addition, the expression levels of miR?518b were highly associated with tumor size, World Health Organization grade and prognosis. Furthermore, overexpression of miR?518b suppressed GBM cell proliferation and angiogenesis, and induced GBM cell apoptosis in vitro and in vivo. Overexpression of miR?518b also inhibited the expression of platelet?derived growth factor receptor ? (PDGFRB), and the present study confirmed that the 3' untranslated region (3'UTR) of PDGFRB was a direct target of miR?518b. In conclusion, to the best of our knowledge, the present study is the first to present evidence suggesting that miR?518b may serve as a potential marker and target in GBM treatment.

SUBMITTER: Xu X

PROVIDER: S-EPMC5647064 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature

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MicroRNA‑518b functions as a tumor suppressor in glioblastoma by targeting PDGFRB.

Xu Xiaolong X Zhang Fenglin F Chen Xianzhen X Ying Qi Q

Molecular medicine reports 20170821 4

Glioblastoma (GBM) is the most common and aggressive type of primary human brain tumor in China. Dysregulated microRNA (miRNA/miR) expression has been hypothesized to serve a role in the tumorigenesis and progression of human GBM. To explore the potential mechanisms affecting GBM tumorigenesis, the function of miR‑518b in regulating GBM cell proliferation and angiogenesis was examined in vitro by CCK‑8 and tube formation assay and in vivo by xenograft assay. The present study demonstrated that t ...[more]

PMID: 28849154

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Project description:BACKGROUND:Discoidin domain receptor-1 (DDR1) tyrosine kinase is highly expressed in a variety of human cancers and involved in various steps of tumorigenesis. However, the precise mechanisms underlying the abnormal expression of DDR1 in oral squamous cell carcinoma (OSCC) has not been well investigated. METHODS:The expression of DDR1 on OSCC patients was determine by quantitative real-time PCR (qRT-PCR) and immunohistochemistry. Specific targeting by miRNAs was determined by software prediction, luciferase reporter assay, and correlation with target protein expression. The functions of miR-486-3p and DDR1 were accessed by MTT and Annexin V analyses using gain- and loss-of-function approaches. Chromatin immunoprecipitation (ChIP) and methylation specific PCR (MSP) were performed to explore the molecular mechanisms by arecoline treatment. RESULTS:Here, we reported that DDR1 was significantly upregulated in OSCC tissues and its levels were inversely correlated with miR-486-3p expression. The experimental results in vitro confirmed that miR-486-3p decreased DDR1 expression by targeting the 3'-UTR of DDR1 mRNA. Overexpression of miR-486-3p led to growth inhibition and apoptosis induction with a similar function by knockdown of DDR1. Aberrant methylation of ANK1 promoter was a highly prevalent in OSCC and contributes to oral carcinogenesis by epigenetic silencing of ANK1 and miR-486-3p. We found that miR-486-3p can be transcriptionally co-regulated with its host gene ANK1 through epigenetic repression. DNA methylation inhibitor treatment re-expressed ANK1 and miR-486-3p. Importantly, arecoline, a major betel nut alkaloid, recruited DNMT3B binding to ANK1 promoter for DNA methylation and then attenuated the expression of miR-486-3p in OSCC. CONCLUSION:This study was the first to demonstrate that betel nut alkaloid may recruit DNMT3B to regulate miR-486-3p/DDR1 axis in oral cancer andmiR-486-3p and DDR1 may serve as potential therapeutic targets of oral cancer.

Dataset Information

MicroRNA?518b functions as a tumor suppressor in glioblastoma by targeting PDGFRB.

Publications

MicroRNA‑518b functions as a tumor suppressor in glioblastoma by targeting PDGFRB.

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