Carvedilol suppresses malignant proliferation of mammary epithelial cells through inhibition of the ROS‑mediated PI3K/AKT signaling pathway

卡维地洛通过抑制 ROS 介导的 PI3K/AKT 信号通路抑制乳腺上皮细胞恶性增殖

阅读:12
作者:Zhongbing Ma, Xingli Liu, Qiang Zhang, Zhigang Yu, Dezong Gao

Abstract

Reactive oxygen species (ROS) cause oncogenic mutations through direct interaction with DNA. Carvedilol (CAR) exhibits antioxidative activity, and pre‑clinical studies have identified that CAR may prevent malignant transformation in certain carcinogenic models. This suggests that CAR may be a potential agent in cancer prevention. In the present study, non‑cancerous MCF‑10A cells were used as a model to investigate the chemopreventive effect of CAR on benzo(a)pyrene (BaP)‑induced cellular carcinogenesis. It was identified that CAR had the ability to eliminate BaP‑induced ROS production and subsequent DNA damage. CAR/BaP activated the ROS‑mediated phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT)Thr308 signaling pathway, whereas the effectors of the PI3K/AKT signaling pathway, murine double minute 2 (MDM2) and p53Ser15, served important functions in the BaP/CAR‑mediated MCF10A cellular transformation. The results of the present study indicated that CAR may be a novel chemopreventive agent, notably in the prevention of estrogen receptor‑negative breast cancer. The antioxidant effects of CAR may contribute to its chemopreventive activity.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。