Ai Hongyan, Zhou Wei, Wang Zeqiang, Qiong Guo, Chen Zhouxi, Deng Shungang
Department of Breast surgery, Zhuzhou City Central Hospital, Xiangya Medical College, Certral South University, Zhuzhou, China.
Department of General surgery, Zhuzhou City Central Hospital, Xiangya Medical College, Certral South University, Zhuzhou, China.
J Cell Biochem. 2019 May;120(5):8696-8705. doi: 10.1002/jcb.28157. Epub 2018 Dec 2.
To investigate the effects of microRNAs-107 (miR-107) on autophagy, proliferation, and migration of breast cancer cells and its mechanism by targeting high mobility group protein B1 (HMGB1).
Real-time polymerase chain reaction assay was used to detect the expression of miR-107 in breast cancer and its cell lines. In MDA-MB-231 and MDA-MB-453 breast cancer cells, the expression of p62, Beclin1 protein, and the changes of cell proliferation and migration after overexpression of m miR-107 were detected by Western blotting, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, and transwell assays. Target Scan online prediction, dual luciferase reporter gene, and Western blot were used to verify the targeting relationship between miR-107 and HMGB1. The effects of silencing HMGB1 expression on p62, Beclin1 protein expression, cell proliferation, and migration ability were detected. The transfected MDA-MB-453 cells were inoculated into the right axilla of the nude mice, the tumor volume and weight were weighed, and the expression of miR-107, HMGB1, p62, and Beclin1 in the tumor were detected.
The expression of miR-107 was downregulated in breast cancer tissues and cell lines (P < 0.01). The expression of p62 protein was upregulated (P < 0.01), while Beclin1 protein was downregulated (P < 0.01) and cell proliferation and migration ability were decreased (P < 0.01) after overexpressing miR-107 in MDA-MB-231 and MDA-MB-453 cells. The results of TargetScan online prediction, dual luciferase reporter gene, and Western blot showed that miR-107 could regulate HMGB1 expression. The expression of p62 protein was upregulated (P < 0.01), while Beclin1 protein was downregulated (P < 0.01) and cell proliferation and migration ability were decreased (P < 0.01) after silencing HMGB1 in MDA-MB-231 and MDA-MB-453 cells. The results of xenograft experiments showed that miR-107 could delay tumor growth and inhibit autophagy.
miR-107 could inhibit cell autophagy, proliferation, and migration of breast cancer cells by targeting HMGB1.
探讨微小RNA-107（miR-107）通过靶向高迁移率族蛋白B1（HMGB1）对乳腺癌细胞自噬、增殖及迁移的影响及其机制。
采用实时聚合酶链反应检测乳腺癌组织及其细胞系中miR-107的表达。在MDA-MB-231和MDA-MB-453乳腺癌细胞中，通过蛋白质免疫印迹法、3-(4,5-二甲基噻唑-2)-2,5-二苯基四氮唑溴盐法和Transwell实验检测过表达miR-107后p62、Beclin1蛋白的表达以及细胞增殖和迁移的变化。利用Target Scan在线预测、双荧光素酶报告基因实验和蛋白质免疫印迹法验证miR-1
