解放军医学院学报2024，Vol.45Issue(9)：960-968,9.DOI:10.12435/j.issn.2095-5227.2024.119
circRNA-PTPRM靶向miR-139-5p调控肝癌细胞增殖、迁移和侵袭的研究
circRNA-PTPRM targeting miR-139-5p regulates proliferation,migration,and invasion of liver cancer cells
摘要
Abstract
Background Inhibiting aberrantly activated signaling pathways can effectively inhibit the growth and proliferation of tumor cells,which provides a new idea for the treatment of liver cancer.Objective To investigate the impact of circRNA-PTPRM on liver cancer cell proliferation,migration,and invasion.Methods qRT-PCR was used to detect the expression levels of PTPRM and miR-139-5p in normal liver cell line HL-7702 and liver cancer cell lines HepG2,Hep3B,Huh-7.Bioinformatics and dual luciferase assays were used to verify the interaction between PTPRM and miR-139-5p.Cell proliferation was assessed using MTT assay,while Transwell experiments were used to evaluate cell migration and invasion.Western blotting was applied to analyze the protein expression related to cell proliferation and invasion.Results PTPRM levels were higher and miR-139-5p levels were lower in HepG2,Hep3B,and Huh-7 cell lines compared to normal liver HL-7702 cells(P<0.05).HepG2 was used for further experiments.Bioinformatics and experimental data confirmed PTPRM's regulatory effect on miR-139-5p expression.PTPRM upregulation negated miR-139-5p's suppressive effects on liver cancer cell proliferation,migration,and invasion.Conversely,silencing PTPRM could increase miR-139-5p levels and reduce hepatocellular carcinoma cell proliferation,migration,invasion,and Cyclin D1 expression.Conclusion Silencing PTPRM potentially elevates miR-139-5p expression,resulting in decrease of proliferation,migration,and invasion of liver cancer cells.关键词
circRNA-PTPRM/miR-139-5p/肝癌细胞/基因调控/增殖/侵袭/迁移Key words
circRNA-PTPRM/miR-139-5p/liver cancer cells/gene regulation/proliferation/invasion/migration分类
医药卫生引用本文复制引用
陈秀华,吴健晖,陈良,陈小芳,余婷,许芝彬..circRNA-PTPRM靶向miR-139-5p调控肝癌细胞增殖、迁移和侵袭的研究[J].解放军医学院学报,2024,45(9):960-968,9.基金项目
海南省卫生健康行业科研项目(22A200192) （22A200192）
