Effects of genistein on apoptosis and EGFR/PI3K/Akt signal transductionpathway in triple-negative breast cancer MDA-MB-231 cells
10.3969/j.issn.1001-1978.2017.10.010
- VernacularTitle:金雀异黄酮对三阴乳腺癌MDA-MB-231细胞凋亡及EGFR/PI3K/Akt通路的影响
- Author:
Liqun WEI
;
Wanting LI
;
Tong LI
;
Chengfei XU
;
Shuangyi TANG
;
Jialiang GAN
- Keywords:
genistein;
triple-negative breast cancer;
apoptosis;
proliferation;
epidermal growth factor receptor;
EGFR/PI3K/Akt signaling pathway
- From:
Chinese Pharmacological Bulletin
2017;33(10):1376-1381
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effect of genistein on apoptosis in triple-negative breast cancer MDA-MB-231 cells and the underlying mechanisms.Methods MTT assay was used to detect the inhibition rate on breast cancer MDA-MB-231 cells of genistein.Hoechst 33258 staining was applied to determine the effect of genistein on morphology of MDA-MB-231 cells.qRT-PCR was employed to detect the mRNA expression of EGFR in MDA-MB-231 cells.Western blot was utilized to determine the expression of Bcl-2, Bax, caspase-3, EGFR, Akt, and p-Akt.The expressions of Akt and p-Akt proteins in breast cancer MDA-MB-231 cells were detected after treated with Akt activator insulin, genistein and in combination with insulin.Results Genistein inhibited the viability of breast cancer MDA-MB-231 cells in a time-dependent manner.The results of Hoechst 33258 staining showed a typical apoptotic morphological changes of MDA-MB-231 cells after treatment of genistein for 36 h.qRT-PCR showed that the mRNA expression of EGFR in MDA-MB-231 cells decreased after treated with genistein for 36 h.The expression levels of Bcl-2, EGFR, Akt, p-Akt, ERK, p-ERK were significantly down-regulated(P<0.01) compared with control.While, the expression of Bax, caspase-3 was significantly up-regulated (P<0.01).It was observed that p-Akt was significantly activated after the treatment of Akt activator insulin (P<0.01), however, significantly down-regulated (P<0.01) when treated with genistein.Conclusion Genistein could inhibit the growth of triple-negative breast cancer MDA-MB-231 cells and induce apoptosis, which probably involves regulating EGFR/PI3K/Akt signaling pathway.
