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MBC in Press, published online ahead of print January 5, 2005
Mol. Biol. Cell 10.1091/mbc.E04-10-0906

A more recent version of this article appeared on March 1, 2005
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Submitted on October 18, 2004
Accepted on December 16, 2004

Selective Inactivation of a FADD-dependent Apoptosis and Autophagy Pathway in Immortal Epithelial Cells

Jacqueline Thorburn,* Franklin Moore, Anuradha Rao, Wendy W. Barclay, Lance R. Thomas, Ken W. Grant, Scott D. Cramer, and Andrew Thorburn{dagger}

Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157

Monitoring Editor: Gerard Evan

Although evasion of apoptosis is thought to be required for the development of cancer, it is unclear which cell death pathways are evaded. We previously identified a novel epithelial cell death pathway that works in normal cells but is inactivated in tumor cells implying that it may be targeted during tumor development. The pathway can be activated by the death domain of the adaptor protein FADD but is distinct from the known mechanism of FADD-induced apoptosis through caspase-8. Here we show that a physiological signal (Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand, TRAIL) can kill normal epithelial cells through the endogenous FADD protein using the novel FADD death domain pathway, which activates both apoptosis and autophagy. We also show that selective resistance to this pathway occurs when primary epithelial cells are immortalized and that this occurs through a mechanism that is independent of known events (telomerase activity, and loss of function of p53, Rb, INK4a and ARF) that are associated with immortalization. These data identify a novel cell death pathway that combines apoptosis and autophagy and is selectively inactivated at the earliest stages of epithelial cancer development.

*Present address: Dept. of Pharmacology, University of Colorado Health Sciences Center, UCHSC at Fitzsimmons, P.O. Box 6511, Mail Stop 8303, Aurora, CO 80045-0511.

{dagger}Corresponding author. E-mail: Andrew.Thorburn{at}uchsc.edu




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