Section 73
Chapter 72,900

MiR-146b promotes cell proliferation and increases chemosensitivity, but attenuates cell migration and invasion via FBXL10 in ovarian cancer

Yan, M.; Yang, X.; Shen, R.; Wu, C.; Wang, H.; Ye, Q.; Yang, P.; Zhang, L.; Chen, M.; Wan, B.; Zhang, Q.; Xia, S.; Lu, X.; Shao, G.; Zhou, X.; Yu, J.; Shao, Q.

Cell Death and Disease 9(11): 1123


PMID: 30409964
DOI: 10.1038/s41419-018-1093-9
Accession: 072899118

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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.

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