Differential requirement for MEK Partner 1 in DU145 prostate cancer cell migration

ERK signaling regulates focal adhesion disassembly during cell movement, and increased ERK signaling frequently contributes to enhanced motility of human tumor cells. We previously found that the ERK scaffold MEK Partner 1 (MP1) is required for focal adhesion disassembly in fibroblasts. Here we test...

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Bibliographic Details
Published in:Cell communication and signaling 2009-11, Vol.7 (1), p.26-26, Article 26
Main Authors: Park, Electa R, Pullikuth, Ashok K, Bailey, Evangeline M, Mercante, Donald E, Catling, Andrew D
Format: Article
Language:English
Subjects:
Cancer cells
Cellular signal transduction
Physiological aspects
Protein kinases
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Summary:ERK signaling regulates focal adhesion disassembly during cell movement, and increased ERK signaling frequently contributes to enhanced motility of human tumor cells. We previously found that the ERK scaffold MEK Partner 1 (MP1) is required for focal adhesion disassembly in fibroblasts. Here we test the hypothesis that MP1-dependent ERK signaling regulates motility of DU145 prostate cancer cells. We find that MP1 is required for motility on fibronectin, but not for motility stimulated by serum or EGF. Surprisingly, MP1 appears not to function through its known binding partners MEK1 or PAK1, suggesting the existence of a novel pathway by which MP1 can regulate motility on fibronectin. MP1 may function by regulating the stability or expression of paxillin, a key regulator of motility.
ISSN:1478-811X
1478-811X
DOI:10.1186/1478-811X-7-26