Open AccessFOXP 3 inhibits MYC expression via regulating miR‐198 and influences cell viability, proliferation and cell apoptosis in HepG2
Author(s) -
Duan Xiaohui,
Jiang Bo,
Yang Jianhui,
Zhou Lixue,
Tian Bingzhang,
Mao Xianhai
Publication year - 2018
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.1780
Subject(s) - downregulation and upregulation , cell growth , cancer research , biology , apoptosis , cell , flow cytometry , oncogene , microbiology and biotechnology , gene , cell cycle , genetics
Abstract Objective Our study aimed to explore the effects of FOXP 3 expression on liver neoplasms cells and to further investigate the relationship between FOXP 3 and proto‐oncogene MYC . Methods QRT ‐ PCR was used for assessment of FOXP 3 expression in liver neoplasms tissues and para‐carcinoma tissues. The effects of FOXP 3 on cell viability were determined by CCK 8 assay, clone formation experiment, and flow cytometry. For mi RNA selection, chips were used to figure out the differentially expressed mi RNA s in FOXP 3‐overexpressing HepG2 cells. The result was followed by bioinformatics prediction to screen the possible MYC ‐targeted mi RNA s, and it was examined by dual luciferase assay and Ch IP assay. The expression levels of MYC protein and apoptosis‐associated proteins (bcl2 and bax) were measured by Western blot assay. Results It showed an under‐regulated expression of FOXP 3 in liver neoplasm tissues from qRT ‐ PCR results. Overexpression of FOXP 3 contributed to cell apoptosis as well as suppressed tumor cells’ proliferation. MiR‐198 was detected to be highly expressed in FOXP 3‐overexpressing HepG2 cells. FOXP 3 regulated the transcription level of miR‐198 by binding to its promoter sequence and overexpressed miR‐198 could suppress tumor cells’ proliferation and promote cell apoptosis. There existed targeted relationship between miR‐198 and MYC gene. MiR‐198 inhibited cancer by suppressing the expression of MYC in liver neoplasm. Conclusion FOXP 3 up‐regulated miR‐198 expression by binding to its promoter sequence specifically, while miR‐198 inhibited proto‐oncogene MYC via targeted relationship. High level of miR‐198 contributed to the apoptosis of tumor cells and suppressed cell viability meanwhile.