Dataset Information

Downregulation of N⁶-methyladenosine binding YTHDF2 protein mediated by miR-493-3p suppresses prostate cancer by elevating N⁶-methyladenosine levels.

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

SUBMITTER: Li J

PROVIDER: S-EPMC5790497 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature

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

Li Jiangfeng J Meng Shuai S Xu Mingjie M Wang Song S He Liujia L Xu Xin X Wang Xiao X Xie Liping L

Oncotarget 20171218 3

Recent evidence suggests that m6A modifications regulate the progressions of several types of tumors. YTHDF2, an m6A reader, has been implicated in the regulation of hepatocellular carcinoma (HCC). miR-493-3p has been defined as tumor suppressor that inhibits the progressions of several types of cancers. However, the functions and mechanisms of YTHDF2 and the indirect m6A regulated role of miR-493-3p in prostate cancer (PCa) remains to be elusive. In this study, immuno-histochemical (IHC) staini ...[more]

PMID: 29423080

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Dataset Information

Downregulation of N⁶-methyladenosine binding YTHDF2 protein mediated by miR-493-3p suppresses prostate cancer by elevating N⁶-methyladenosine levels.

Publications

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

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Dataset Information

Downregulation of N6-methyladenosine binding YTHDF2 protein mediated by miR-493-3p suppresses prostate cancer by elevating N6-methyladenosine levels.

Publications

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

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

Downregulation of N⁶-methyladenosine binding YTHDF2 protein mediated by miR-493-3p suppresses prostate cancer by elevating N⁶-methyladenosine levels.