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[Cancer Research 61, 6569-6576, September 1, 2001]
© 2001 American Association for Cancer Research

Tumor Biology

Activation of Extracellular Signal-regulated Kinase and c-Jun-NH2-terminal Kinase but not p38 Mitogen-activated Protein Kinases Is Required for RRR-{alpha}-Tocopheryl Succinate-induced Apoptosis of Human Breast Cancer Cells1

Weiping Yu, Qiao Yin Liao, Feras M. Hantash, Bob G. Sanders and Kimberly Kline2

Division of Nutrition/A2703 [W. Y., Q. Y. L., F. M. H., B. G. S., K. K.] and School of Biological Sciences [W. Y., Q. Y. L., F. M. H., B. G. S.], University of Texas at Austin, Austin, Texas 78712

RRR-{alpha}-tocopherol succinate (vitamin E succinate, VES) is a potent, selective apoptotic agent for cancer cells but not normal cells. VES has been shown to inhibit the growth of a wide variety of tumor cells in cell culture and animal models. Studies addressing mechanisms of action of VES-induced apoptosis have identified transforming growth factor-ß, Fas/CD95-APO-1, and mitogen-activated protein kinase (MAPK) signaling pathway involvement. Here we show that MAPKs, the extracellular signal-regulated kinases (ERK), and the stress-activated protein kinases, c-Jun NH2-terminal kinases (JNK), but not p38, are critical mediators in VES-induced apoptosis of human breast cancer MDA-MB-435 cells. VES activates ERK1/2 and JNK both in level and duration of kinase activity. Expression of dominant negative mutants of ERK1, MAPK/ERK activator-1, or JNK1 but not p38 blocked phosphorylation of the substrate glutathione S-transferase-c-Jun and inhibited VES-induced apoptosis. Increased phosphorylation and transactivation activity of nuclear transcription factors c-Jun, ATF-2, and Elk-1 are observed after VES treatments; however, only c-Jun and ATF-2 appear to be involved in VES-induced apoptosis based on antisense blockage experiments. Collectively, these results imply a critical role for ERK1 and JNK1 but not p38 in VES-induced apoptosis of human MDA-MB-435 breast cancer cells.




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Copyright © 2001 by the American Association for Cancer Research.