MiR-146b promotes cell proliferation and increases chemosensitivity, but attenuates cell migration and invasion via FBXL10 in ovarian cancer. Issue 11 (November 2018)

• Record Type: Journal Article
• Authors: Yan, Meina; Yang, Xinxin; Shen, Rong; Wu, Chengjiang; Wang, Hui; Ye, Qing; Yang, Peifang; Zhang, Lubin; Chen, Miao; Wan, Bing; Zhang, Qinqin; Xia, Sheng; Lu, Xiaodong; Shao, Genbao; Zhou, Xiaoming; Yu, Jun; Shao, Qixiang
• Is Part Of: Cell death and disease. Volume 9:Issue 11(2018)
• Page Start: 1
• Page End: 17
• Publication Date: 2018-11
• Subjects: Cell death -- Periodicals; Apoptosis -- Periodicals; 571.936
• DOI: 10.1038/s41419-018-1093-9
• Languages: English
• ISSNs: 2041-4889

Abstract

Abstract Epithelial ovarian carcinoma (EOC) is the most lethal gynecologic malignancy. However, the molecular mechanisms remain unclear. In this study, we found that miR-146b was downregulated in EOC and its expression level was negatively correlated with the pathological staging. Follow-up functional experiments illustrated that overexpression of miR-146b significantly inhibited cell migration and invasion, and increased cell proliferation, but it also improved the response to chemotherapeutic agents. Mechanistically, we demonstrated that miR-146b exerted its function mainly through inhibiting F-box and leucine-rich repeat protein 10 (FBXL10), and upregulated the Cyclin D1, vimentin (VIM), and zona-occludens-1 (ZO-1) expression in EOC. These findings indicate that miR-146b–FBXL10 axis is an important epigenetic regulation pathway in EOC. Low miR-146b may contribute to cancer progression from primary stage to advanced stage, and may be the promising therapeutic target of EOC.