Abstract | BACKGROUND: METHODS: Plasma miRNA expression profiles were compared between healthy people and CRC patients. MiRNA expression was measured using quantitative real-time PCR. Colony formation and MTT assays were used to test cell proliferation. Luciferase assay, immunohistochemistry and Western blotting were employed to explore the molecular mechanism. RESULTS: MiR-142-3p level was found as the most significantly repressed miRNA in CRC patients. Overexpression of miR-142-3p dramatically repressed colony formation and cell proliferation of both HT29 and HCT116 cells while inhibition of miR-142-3p promoted those of the cells. Interestingly, overexpression of miR-142-3p reduced the level and nuclear accumulation of β- catenin. We further observed that miR-142-3p remarkably inhibited the transcriptional activity of β- catenin gene (CTNNB1). However, mutations in the predicted binding sites blocked this inhibition, suggesting that miR-142-3p may directly bind to the mRNA of β- catenin. CONCLUSION: In conclusion, we identified miR-142-3p exerts its function as a tumor suppressor through blocking the activation of Wnt signaling by directly targeting to CTNNB1.
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Authors | Peng Liu, Fuao Cao, Jinke Sui, Yonggang Hong, Qizhi Liu, XianHua Gao, Haifeng Gong, Liqiang Hao, Zheng Lou, Wei Zhang |
Journal | Frontiers in oncology
(Front Oncol)
Vol. 10
Pg. 552944
( 2020)
ISSN: 2234-943X [Print] Switzerland |
PMID | 33643894
(Publication Type: Journal Article)
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Copyright | Copyright © 2021 Liu, Cao, Sui, Hong, Liu, Gao, Gong, Hao, Lou and Zhang. |