大黄素通过调节miR-582-3p影响MAP3K1活性抑制乳腺癌细胞增殖并诱导凋亡[1]

目的:探究大黄素通过microRNA (miR)-582-3p/MAP3K1对乳腺癌细胞增殖、凋亡的作用及分子机制。方法:检测大黄素及miR-582-3p异常表达对乳腺癌细胞增殖及凋亡的影响。qRT-PCR检测miR-582-3p及MAP3K1的表达。MTT检测乳腺癌细胞增殖,流式细胞术和TUNEL实验检测细胞凋亡。western blot检测增殖标志蛋白Ki-67及凋亡标志蛋白Bcl-2、Bax和Caspase-3在癌细胞中的表达水平。结果:大黄素可以抑制乳腺癌细胞MCF-7及MDA-MB-231的增殖能力及促进凋亡。western blot结果显示大黄素会抑制细胞中Ki-67及Bcl-2的表达并促进Caspase-3 (cleaved)及Bax的表达。大黄素处理乳腺癌细胞后miR-582-3p的表达显著下调。过表达miR-582-3p会下调大黄素对乳腺癌细胞生物学活性的影响。大黄素还会通过miR-583-3p调节癌细胞中MAP3K1的表达。结论:大黄素通过调节miR-582-3p影响MAP3K1活性抑制乳腺癌细胞增殖并诱导凋亡。

Emodin inhibits Breast cancer cells proliferation and induces apoptosis through downregulation of miR-582-3p that suppresses MAP3K1FAN Minhui1,SHUAI Renya1,Li Qingyu2

Aim: To investigate the role and molecular mechanisms of Emodin on proliferation and apoptosis of breast cancer cells via microRNA (miR)-582-3p/MAP3K1. Methods: The effects of Emodin and miR-582-3p on proliferation and apoptosis of breast cancer cells were assessed. Cell proliferation and apoptosis were examined by MTT, flow cytometry and TUNEL experiment. The levels of miR-582-3p and MAP3K1 were examined by qRT-PCR. The protein expression levels of proliferation and apoptosis markers were assessed by western blot. Results: Emodin suppressed proliferation and promoted apoptosis of MCF cells and MDA-MB-231 cells. The levels of Ki-67 and Bcl-2 protein were upregulation and the levels of Caspase-3 (cleaved) and Bax protein were downregulation by Emodin treatment. The expression of miR-582-3p was significantly down-regulated after Emodin treatment of cancer cells. Overexpression of miR-582-3p inhibited the effect of Emodin on biological activity of cancer cells. Emodin could also regulate the expression of MAP3K1 via miR-583-3p in breast cancer cells. Conclusion: Emodin could inhibit Breast cancer cell proliferation and induce apoptosis through downregulation of miR-582-3p that suppresses MAP3K1.