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Involvement of JNK/p73/NOXA in vitamin E analog-induced apoptosis of human breast cancer cells

✍ Scribed by Pei Wang; Weiping Yu; Zhanzhi Hu; Li Jia; Vishwanath R. Iyer; Bob G. Sanders; Kimberly Kline

Publisher
John Wiley and Sons
Year
2008
Tongue
English
Weight
221 KB
Volume
47
Category
Article
ISSN
0899-1987

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✦ Synopsis

Abstract

Microarray analyses of human MDA‐MB‐435 breast cancer cells treated with vitamin E analog 2,5,7,8‐tetramethyl‐2R‐(4R,8R,12‐trimethyltridecyl) chroman‐6‐yloxy acetic acid (α‐TEA) showed over 400 genes to be modulated. Thirty‐four genes deemed of interest based on potential involvement in anticancer activities of α‐TEA fell into six categories: apoptosis related, signal transduction, cell cycle related, cell adhesion and motility, transcriptional regulators, and membrane traffic related. The gene (PMAIP1) for NOXA was studied further. NOXA mRNA and protein levels were elevated in a time and dose‐dependent fashion following α‐TEA treatment. Functional knockdowns using small interfering RNA (siRNA) showed NOXA to contribute to α‐TEA‐induced apoptosis. A correlation between α‐TEA's ability to upregulate NOXA and induce apoptosis was seen among several human breast cancer cell lines. Efforts to identify upstream regulators of NOXA in α‐TEA‐induced apoptosis identified the necessity of both c‐Jun N‐terminal kinase (JNK) activation and p73 expression. Additionally, protein levels of full length p73 were decreased by JNK siRNA treatment, suggesting that the signal transduction module of JNK‐p73‐NOXA is involved in α‐TEA induced apoptosis of human breast cancer cells. Taken together, these findings suggest a role for JNK activation in mediating full length p73 expression and add to our understanding of the mechanisms of anticancer actions of α‐TEA, a potential chemotherapeutic agent. © 2007 Wiley‐Liss, Inc.

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