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Evidence-Based Complementary and Alternative Medicine
Volume 2013, Article ID 429393, 12 pages
http://dx.doi.org/10.1155/2013/429393
Research Article

Antiproliferative Action of Conjugated Linoleic Acid on Human MCF-7 Breast Cancer Cells Mediated by Enhancement of Gap Junctional Intercellular Communication through Inactivation of NF-κB

1Division of Applied Life Sciences (BK21 Plus), Graduate School, and Institute of Agriculture & Life Science, Gyeongsang National University, Jinju 660-701, Republic of Korea
2Department of Biochemistry and Molecular Biology, Faculty of Science, University of Rajshahi, Rajshahi-6205, Bangladesh
3Department of Internal Medicine and Institute of Health Sciences, Gyeongsang National University, School of Medicine, Jinju 660-702, Republic of Korea
4Laboratory of Biochemistry (BK21 Plus), School of Veterinary Medicine, Gyeongsang National University, Jinju 660-701, Republic of Korea
5Department of Physiology and Institute of Health Sciences, Gyeongsang National University, School of Medicine, Jinju 660-702, Republic of Korea
6HK Biotech Co., Ltd., Jinju 660-844, Republic of Korea

Received 7 September 2013; Accepted 1 November 2013

Academic Editor: Shuang-En Chuang

Copyright © 2013 Md. Abdur Rakib et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The major conjugated linoleic acid (CLA) isomers, c9,t11-CLA and t10,c12-CLA, have anticancer effects; however, the exact mechanisms underlying these effects are unknown. Evidence suggests that reversal of reduced gap junctional intercellular communication (GJIC) in cancer cells inhibits cell growth and induces cell death. Hence, we determined that CLA isomers enhance GJIC in human MCF-7 breast cancer cells and investigated the underlying molecular mechanisms. The CLA isomers significantly enhanced GJIC of MCF-7 cells at 40 μM concentration, whereas CLA inhibited cell growth and induced caspase-dependent apoptosis. CLA increased connexin43 (Cx43) expression both at the transcriptional and translational levels. CLA inhibited nuclear factor-κB (NF-κB) activity and enhanced reactive oxygen species (ROS) generation. No significant difference was observed in the efficacy of c9,t11-CLA and t10,c12-CLA. These results suggest that the anticancer effect of CLA is associated with upregulation of GJIC mediated by enhanced Cx43 expression through inactivation of NF-κB and generation of ROS in MCF-7 cells.