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目的观察染料木黄酮(GEN)对HER2/neu高表达人乳腺癌MDA-MB-453细胞PI3K/Akt信号途径的抑制作用,探讨其在GEN增敏阿霉素(DOX)体外化疗乳腺癌MDA-MB-453细胞中的作用。方法GEN、PI3K特异性抑制剂渥曼青霉素(WT)和DOX单独或联合处理体外培养的MDA-MB-453细胞,免疫细胞化学法检测HER-2/neu蛋白表达,免疫印迹法检测总Akt和磷酸化Akt蛋白(p-Akt)表达。结果GEN对MDA-MB-453细胞HER2/neu和总Akt蛋白没有明显影响,但可明显降低p-Akt蛋白水平;同时WT也能明显降低p-Akt蛋白,并显著增强DOX抑制MDA-MB-453细胞生长的作用。结论GEN增敏DOX体外化疗乳腺癌MDA-MB-453细胞株可能与其抑制PI3K/Akt信号途径有关。
Objective To investigate the inhibitory effect of genistein on the PI3K / Akt signaling pathway in HER2 / neu overexpressing human breast cancer cell line MDA-MB-453 and to explore the role of genistein in the proliferation of breast cancer MDA- MB-453 cells. Methods GEN, PI3K-specific inhibitor wortmannin (WT) and DOX, alone or in combination, were used to treat MDA-MB-453 cells cultured in vitro. The expression of HER-2 / neu protein was detected by immunocytochemistry. Phosphorylated Akt protein (p-Akt) expression. Results GEN had no significant effect on the expression of HER2 / neu and total Akt in MDA-MB-453 cells, but significantly decreased the level of p-Akt protein. Meanwhile, WT also significantly decreased p-Akt protein and markedly enhanced the inhibitory effect of DOX on MDA- 453 cell growth. Conclusion GEN sensitized DOX may be related to its inhibition of PI3K / Akt signaling pathway in vitro.