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First published online September 18, 2007
doi: 10.1242/10.1242/jcs.010389

Journal of Cell Science 120, 3163-3172 (2007)
Published by The Company of Biologists 2007
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Commentary

The RASSF1A tumor suppressor

Howard Donninger1, Michele D. Vos2 and Geoffrey J. Clark1,*

1 Molecular Targets Group, Department of Medicine, J. G. Brown Cancer Center, University of Louisville, 119C Baxter Boulevard, 580 S. Preston Street, Louisville, KY 40202, USA
2 Research Analysis and Evaluation Branch, NCI, Rockville, MD, USA

* Author for correspondence (e-mail: gjclar01{at}louisville.edu)

Accepted 23 July 2007

RASSF1A (Ras association domain family 1 isoform A) is a recently discovered tumor suppressor whose inactivation is implicated in the development of many human cancers. Although it can be inactivated by gene deletion or point mutations, the most common contributor to loss or reduction of RASSF1A function is transcriptional silencing of the gene by inappropriate promoter methylation. This epigenetic mechanism can inactivate numerous tumor suppressors and is now recognized as a major contributor to the development of cancer.

RASSF1A lacks apparent enzymatic activity but contains a Ras association (RA) domain and is potentially an effector of the Ras oncoprotein. RASSF1A modulates multiple apoptotic and cell cycle checkpoint pathways. Current evidence supports the hypothesis that it serves as a scaffold for the assembly of multiple tumor suppressor complexes and may relay pro-apoptotic signaling by K-Ras.

Key words: Epigenetic, RASSF1A, Ras, Tumor suppressor




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