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Published:
Oct 4, 2017Keywords:
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Main Article Content
MiR-495-3p facilitates colon cancer cell proliferation via Wnt/β-catenin signaling pathway by restraining Wnt inhibitory factor
Abstract
Purpose: To demonstrate whether miR-495-3p promote the occurrence of colon cancer and development of colon cancer stem cells by inhibiting Wnt inhibitory factor (WIF1).
Methods: The level of MiRNA and mRNA in cells were tested by real-time polymerase chain reaction (RT-PCR). Cell viability was assessed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Cell spheroid formation was measured by colony assay. Expression protein was tested using Western blotting. β-catenin binding ability was detected by chromatin immunoprecipitation (ChIP) assay. MiRNA target gene was defined by luciferase assay.
Results: Compared with normal colon cells and tissue, miR-495-3p is elevated in colon cancer cells and tissues, which regulate proliferation, level of stemness factors SOX-9, Bmil, and OCT-4 in HCT-116 cells, even spheroid formation. Overexpression of miR-495-3p inhibits the expression of WIF1 in HCT-116 cells and promotes colon tumorigenesis by binding with 3’-UTR. MiR-495-3p inhibitor downregulated WIF1-enhanced sphere formation of colon cancer cells.
Conclusion: These results indicate that miR-495-3p/WIF1 can modulate the development of colon cancer and is a potential target for prevention and treatment of cancer.
Keywords: MiR-495-3p, Wnt inhibitory factor, Colon cancer, Stemness, Tumorigenesis
