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共轭亚油酸通过抑制 NF-κB 增强细胞间隙连接通讯对人 MCF-7 乳腺癌细胞的增殖抑制作用。

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- κ B.

机构信息

Division of Applied Life Sciences (BK21 Plus), Graduate School, and Institute of Agriculture & Life Science, Gyeongsang National University, Jinju 660-701, Republic of Korea ; Department of Biochemistry and Molecular Biology, Faculty of Science, University of Rajshahi, Rajshahi-6205, Bangladesh.

Department of Internal Medicine and Institute of Health Sciences, Gyeongsang National University, School of Medicine, Jinju 660-702, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2013;2013:429393. doi: 10.1155/2013/429393. Epub 2013 Nov 25.

DOI:10.1155/2013/429393
PMID:24371460
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3858871/
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  μ M 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- κ B (NF- κ B) 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- κ B and generation of ROS in MCF-7 cells.

摘要

主要的共轭亚油酸（CLA）异构体，c9,t11-CLA 和 t10,c12-CLA，具有抗癌作用；然而，这些作用的确切机制尚不清楚。有证据表明，逆转癌细胞中减少的间隙连接细胞间通讯（GJIC）可抑制细胞生长并诱导细胞死亡。因此，我们确定 CLA 异构体可增强人 MCF-7 乳腺癌细胞中的 GJIC，并研究其潜在的分子机制。CLA 异构体在 40μM 浓度时可显著增强 MCF-7 细胞的 GJIC，而 CLA 则抑制细胞生长并诱导半胱天冬酶依赖性细胞凋亡。CLA 可在转录和翻译水平上增加连接蛋白 43（Cx43）的表达。CLA 抑制核因子- κ B（NF- κ B）活性并增强活性氧（ROS）的产生。c9,t11-CLA 和 t10,c12-CLA 的效果没有明显差异。这些结果表明，CLA 的抗癌作用与通过 NF- κ B 失活和 MCF-7 细胞中 ROS 的产生增强 Cx43 表达介导的 GJIC 上调有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1263/3858871/5266315ff200/ECAM2013-429393.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1263/3858871/af1fa1a728ab/ECAM2013-429393.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1263/3858871/fc41112efd8f/ECAM2013-429393.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1263/3858871/e582a4ff8c67/ECAM2013-429393.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1263/3858871/d2b0c2597c1a/ECAM2013-429393.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1263/3858871/61b6757d84bb/ECAM2013-429393.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1263/3858871/119c2708b05a/ECAM2013-429393.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1263/3858871/5266315ff200/ECAM2013-429393.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1263/3858871/af1fa1a728ab/ECAM2013-429393.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1263/3858871/fc41112efd8f/ECAM2013-429393.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1263/3858871/e582a4ff8c67/ECAM2013-429393.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1263/3858871/d2b0c2597c1a/ECAM2013-429393.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1263/3858871/61b6757d84bb/ECAM2013-429393.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1263/3858871/119c2708b05a/ECAM2013-429393.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1263/3858871/5266315ff200/ECAM2013-429393.007.jpg

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