Skip to main content
. 2021 Jun 17;14:3769–3781. doi: 10.2147/OTT.S275322

Figure 5.

Figure 5

BGM targets Cyclin D1 by up-regulating the expression of miR-145. (A) The WM239 and MM200 cells were treated with BGM at the indicated dose. The expression of miR-145 was measured by qPCR assays in the cells. (B) The WM239 and MM200 cells were treated with miR-145 inhibitor. The expression of miR-145 was measured by qPCR assays in the cells. (C) The WM239 and MM200 cells were treated with BGM at indicated dose, control inhibitor, or co-treated with BGM and miR-145 inhibitor. The cell apoptosis was measure by flow cytometry analysis in the cells. (D) The interaction of miR-145 and Cyclin D1 3ʹ UTR was identified by bioinformatic analysis using Targetscan (http://www.targetscan.org/vert_72/). (E–G) The WM239 and MM200 cells were treated with control mimic or miR-145 mimic. (E) The luciferase activities of wild type Cyclin D1 (Cyclin D1 WT) and Cyclin D1 with the miR-145-binding site mutant (Cyclin D1 MUT) were determined by luciferase reporter gene assays in the cells. (F) The mRNA expression of Cyclin D1 was assessed by qPCR assays in the cells. (G) The protein expression of Cyclin D1 and β-actin was tested by Western blot analysis in the cells. The results of Western blot analysis were quantified by ImageJ software. Data are presented as mean ± SEM. Statistic significant differences were indicated: **P < 0.01.