Downregulation of N 6 -methyladenosine binding YTHDF2 protein mediated by miR-493-3p suppresses prostate cancer by elevating N 6 -methyladenosine levels

作者: Jiangfeng Li , Shuai Meng , Mingjie Xu , Song Wang , Liujia He

DOI: 10.18632/ONCOTARGET.23365

关键词: Cancer researchCell growthCISHCell cultureProstate cancerDownregulation and upregulationReporter geneChromogenic in situ hybridizationChemistryCarcinogenesis

摘要: Recent evidence suggests that m6A modifications regulate the progressions of several types tumors. YTHDF2, an reader, has been implicated in regulation hepatocellular carcinoma (HCC). miR-493-3p defined as tumor suppressor inhibits cancers. However, functions and mechanisms YTHDF2 indirect regulated role prostate cancer (PCa) remains to be elusive. In this study, immuno-histochemical (IHC) staining chromogenic situ hybridization (CISH) were performed find was frequently upregulated but downregulated both PCa tissues cell lines (DU-145 PC3) which negatively correlated with each other. Knock down significantly elevated levels, inhibited proliferation migration DU-145 PC3 lines. The dual-luciferase reporter assay confirmed direct target miR-493-3p. addition, forced expression consistently levels knock YTHDF2. contrast, overexpression inhibition conversely reduced levels. Additionally, rescue experiments revealed abrogated suppression induced by si-YTHDF2. To conclude, miR-493-3p, two crucial regulators, are involved progression indirectly modulating view these promising results, may provide new insights into carcinogenesis potential therapeutic targets for PCa.

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