Attenuation of 12-O-Tetradecanoylphorbol-13-acetate (TPA)-Induced Gap Junctional Intercellular Communication (GJIC) Inhibition in MCF-10A Cells by c9,t11-Conjugated Linoleic Acid
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- 作者：Md. Abdur Rakib ; Young S. Kim ; Wook J. Jang ; Byeong D. Choi ; Jeong O. Kim ; Il K. Kong ; Yeong L. Ha
- 刊名：Journal of Agricultural and Food Chemistry
- 出版年：2010
- 出版时间：November 24, 2010
- 年：2010
- 卷：58
- 期：22
- 页码：12022-12030
- 全文大小：1004K
- 年卷期：v.58,no.22(November 24, 2010)
- ISSN：1520-5118
文摘
The protective effect of c9,t11-conjugated linoleic acid (CLA) on the inhibition of gap junctional intercellular communication (GJIC) was examined in a human mammary epithelial cell line (MCF-10A) treated with 12-O-tetradecanoylphorbol-13-acetate (TPA), relative to t10,c12-CLA isomer. TPA inhibited GJIC in a dose-dependent and reversible manner and was associated with connexin 43 phosphorylation. Pretreatment of 20 μM c9,t11-CLA for 24 h prior to 60 nM TPA for 1 h prevented the inhibition of GJIC by reducing the phosphorylation of connexin 43 via suppressing extracellular signal-regulated kinases (ERK1/2) activation. Reactive oxygen species (ROS) accumulation by TPA was attenuated by c9,t11-CLA. The efficacy of c9,t11-CLA in protecting inhibition of GJIC, connexin 43 phosphorylation, and ROS production was superior to that of t10,c12-CLA. These results suggest that c9,t11-CLA, including t10,c12-CLA, prevents the carcinogenesis of MCF-10A cells by protecting down-regulation of GJIC during the cancer promotion stage, and lack of their toxicities could be an excellent indicator for the chemoprevention of breast cancer.