黄芩苷通过上调miR-126诱导乳腺癌细胞凋亡的机制研究

目的 用黄芩苷干预人乳腺癌细胞株MDA-MB-231，观察黄芩苷对乳腺癌细胞增殖、凋亡的影响及作用机制。方法 用qRT-PCR检测miR-126的表达变化，Western-blot检测Bcl-2、Caspase-9、Caspase-3、p-p38和p53的表达，MTT法检测细胞增殖，流式细胞术检测细胞凋亡。结果 miR-126在乳腺癌MDA-MB-231细胞中的表达比正常乳腺细胞低，黄芩苷干预乳腺癌细胞后miR-126上调最为明显（P<0.05）。用miR-126 mimics、miR-126 inhibitors转染乳腺癌细胞，Western-blot显示黄芩苷及miR-126 mimics作用于人乳腺癌细胞后Bcl-2表达水平下降，Caspase-9和Caspase-3的裂解产物、p-p38、p53表达增加，差异有统计学意义（P<0.05）。MTT法显示黄芩苷和miR-126 均可抑制乳腺癌细胞的增殖，流式细胞术显示黄芩苷与miR-126 mimics促进癌细胞凋亡。结论 黄芩苷可以抑制乳腺癌细胞的增殖，促进其凋亡，其机制可能与通过上调miR-126调节凋亡相关基因有关。

Mechanism of Baicalin on the Apoptosis of Breast Cancer Cells by Up-Regulating miR-126

Objective To observe the effect and mechanisim of baicalin on proliferation and apoptosis of breast cancer cell line MDA-MB-231. Methods The expression of miR-126 was detected by qRT-PCR, and the expression of Bcl-2, Caspase-9, Caspase-3, p-p38, p53 was deternined by Western-blot. The cell proliferation was determined by using MTT method and cell apoptosis was detected by flow cytometry. Results The expression of miR-126 in breast cancer MDA-MB-231 cells was lower than that in normal breast cells, and the most obvious increase in miR-126 regulation was the intervention of baicalin in breast cancer cells. MiR-126 mimics, miR-126 inhibitors were transfected into human breast cancer cell. The Western-blot showed that baicalin and the miR-126 mimics increased Bcl-2 expression, reduced Caspase-9 and Caspase-3, p-p38, p53 expressions in human breast cancer cells (P<0.05). The result of MTT method showed that baicalin and miR-126 mimics could inhibit the proliferation of breast cancer cells, flow cytometry showed that baicalin and miR-126 mimics could promote the apoptosis of cancer cells. Conclusion The baicalin could inhibit the proliferation of breast cancer cells, and promote the apoptosis of breast cancer cells. The mechanism may be associated with the regulation of apoptosis related genes by up-regulating miR-126.