Journal
CELL BIOCHEMISTRY AND BIOPHYSICS
Volume 48, Issue 1, Pages 54-72Publisher
HUMANA PRESS INC
DOI: 10.1007/s12013-007-0036-3
Keywords
HEF1/NEDD9/Cas-L; HEF1; NEDD9; Cas-L; metastasis; scaffolding adaptor protein; invasion; mitosis; apoptosis; signal transduction
Funding
- NATIONAL CANCER INSTITUTE [R01CA063366, P30CA006927] Funding Source: NIH RePORTER
- NCI NIH HHS [R01 CA063366-12, R01 CA063366, CA 06927, R01 CA 63366, P30 CA006927] Funding Source: Medline
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Upregulation of the scaffolding protein HEF1, also known as NEDD9 and Cas-L, has recently been identified as a pro-metastatic stimulus in a number of different solid tumors, and has also been strongly associated with pathogenesis of BCR-Abl-dependent tumors. As the evidence mounts for HEF1/NEDD9/Cas-L as a key player in metastatic cancer, it is timely to review the molecular regulation of HEF1/NEDD9/Cas-L. Most of the mortality associated with cancer arises from uncontrolled metastases, thus a better understanding of the properties of proteins specifically associated with promotion of this process may yield insights that improve cancer diagnosis and treatment. In this review, we summarize the extensive literature regarding HEF1/NEDD9/Cas-L expression and function in signaling relevant to cell attachment, migration, invasion, cell cycle, apoptosis, and oncogenic signal transduction. The complex function of HEF1/NEDD9/Cas-L revealed by this analysis leads us to propose a model in which alleviation of cell cycle checkpoints and acquired resistance to apoptosis is permissive for a HEF1/NEDD9/Cas-L-promoted pro-metastatic phenotype.
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