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1 Division of Life Sciences, Hallym University, Chunchon, Korea, Republic of
2 Food Science and Nutrition, Dankook University, Seoul, Korea, Republic of
3 Department of Pathology, Hallym University, Chunchon, Korea, Republic of
4 Department of Biological Science, Sookmyung Women's University, Seoul, Korea, Republic of
5 Department of Molecular Genetics, University of Ilinois College of Medicine, Chicago, Illinois, USA
* To whom correspondence should be addressed. E-mail: jyoon{at}hallym.ac.kr.
Conjugated linoleic acid (CLA) has chemoprotective properties in experimental cancer models and in vitro studies have shown that CLA inhibits HT-29 colon cancer cell growth. ErbB2 and ErbB3 have been implicated in the development of colon cancer and both proteins are expressed at high levels in the HT-29 cell line. Activation of ErbB2/ErbB3 heterodimers is regulated by the ErbB3 ligand heregulin. To examine CLA regulation of HT-29 cell proliferation and apoptosis and the influence of CLA on the ErbB3 signaling pathway, HT-29 cells were cultured in the presence of CLA and/or heregulin. CLA inhibited DNA synthesis and induced apoptosis of HT-29 cells. While addition of heregulin-
led to an increase in cell number, it was not able to counteract the negative growth regulatory effect of CLA. Immunoprecipitation/Western blot studies revealed that CLA inhibited heregulin--stimulated phosphorylation of ErbB2 and ErbB3, recruitment of the p85 subunit of phosphoinositide 3-kinase (PI3K) to the ErbB3 receptor, ErbB3-associated PI3K activities, and phosphorylation of Akt. CLA decreased ErbB2 and ErbB3 mRNA and protein levels in a dose-dependent manner. In conclusion, we demonstrate that CLA inhibits cell proliferation and stimulates apoptosis in HT-29 cells, and that this may be mediated by its ability to downregulate ErbB3 signaling and the PI3K/Akt pathway.
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