标题:Carvedilol suppresses malignant proliferation of mammary epithelial cells through inhibition of the ROS-mediated PI3K/AKT signaling pathway
作者:Ma, Zhongbing; Liu, Xingli; Zhang, Qiang; Yu, Zhigang; Gao, Dezong
作者机构:[Ma, Zhongbing; Zhang, Qiang; Yu, Zhigang; Gao, Dezong] Shandong Univ, Hosp 2, 247 Beiyuan St, Jinan 250033, Shandong, Peoples R China.; [Liu, Xingl 更多
通讯作者:Gao, DZ
通讯作者地址:[Gao, DZ]Shandong Univ, Hosp 2, 247 Beiyuan St, Jinan 250033, Shandong, Peoples R China.
来源:ONCOLOGY REPORTS
出版年:2019
卷:41
期:2
页码:811-818
DOI:10.3892/or.2018.6873
关键词:carvedilol; cancer prevention; reactive oxygen species; phosphoinositide; 3-kinase; protein kinase B signaling pathway
摘要: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 p53(Ser15), 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.
收录类别:SCOPUS;SCIE
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-85058903806&doi=10.3892%2for.2018.6873&partnerID=40&md5=9d03280425b714b320b6dc084accf294
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