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Death receptors and melanoma resistance to apoptosis

Oncogene volume 22, pages 3152–3161 (2003)Cite this article

Abstract

Impaired ability to undergo programmed cell death in response to a wide range of external stimuli acquires melanomas a selective advantage for progression and metastasis as well as their notorious resistance to therapy. Better understanding of mechanisms that govern apoptosis has enabled identification of diverse routes by which melanomas manage to escape stimuli of apoptosis. Changes at genomic, transcriptional and post-translational levels of G-proteins and protein kinases (Ras, B-Raf) and their transcription factor effectors (c-Jun, ATF2, Stat3 and NF-κB) affects TNF, Fas and TRAIL receptors, which play important roles in acquiring melanoma's resistance to apoptosis. Here, we summarize our current understanding of changes that alters the regulation of death receptors during melanoma development.

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Acknowledgements

Support by NCI grants (CA55995 and CA559908 to ZR) and a Sharp Foundation grant (to ZR) is gratefully acknowledged.

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  1. Ruttenberg Cancer Center, Mount Sinai School of Medicine, New York, 10029, NY, USA

    Vladimir N Ivanov, Anindita Bhoumik & Ze'ev Ronai

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Ivanov, V., Bhoumik, A. & Ronai, Z. Death receptors and melanoma resistance to apoptosis. Oncogene 22, 3152–3161 (2003). https://doi.org/10.1038/sj.onc.1206456

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