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

<p>Abstract</p> <p>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 dis...

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Main Authors: Bailey Evangeline M, Pullikuth Ashok K, Park Electa R, Mercante Donald E, Catling Andrew D
Format: Article
Language:English
Published: BMC 2009-11-01
Series:Cell Communication and Signaling
Online Access:http://www.biosignaling.com/content/7/1/26
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author Bailey Evangeline M
Pullikuth Ashok K
Park Electa R
Mercante Donald E
Catling Andrew D
author_facet Bailey Evangeline M
Pullikuth Ashok K
Park Electa R
Mercante Donald E
Catling Andrew D
author_sort Bailey Evangeline M
collection DOAJ
description <p>Abstract</p> <p>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.</p>
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spelling doaj.art-0b3c60a81bd54ba0807695393b84f7a62022-12-22T01:36:47ZengBMCCell Communication and Signaling1478-811X2009-11-01712610.1186/1478-811X-7-26Differential requirement for MEK Partner 1 in DU145 prostate cancer cell migrationBailey Evangeline MPullikuth Ashok KPark Electa RMercante Donald ECatling Andrew D<p>Abstract</p> <p>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.</p>http://www.biosignaling.com/content/7/1/26
spellingShingle Bailey Evangeline M
Pullikuth Ashok K
Park Electa R
Mercante Donald E
Catling Andrew D
Differential requirement for MEK Partner 1 in DU145 prostate cancer cell migration
Cell Communication and Signaling
title Differential requirement for MEK Partner 1 in DU145 prostate cancer cell migration
title_full Differential requirement for MEK Partner 1 in DU145 prostate cancer cell migration
title_fullStr Differential requirement for MEK Partner 1 in DU145 prostate cancer cell migration
title_full_unstemmed Differential requirement for MEK Partner 1 in DU145 prostate cancer cell migration
title_short Differential requirement for MEK Partner 1 in DU145 prostate cancer cell migration
title_sort differential requirement for mek partner 1 in du145 prostate cancer cell migration
url http://www.biosignaling.com/content/7/1/26
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AT pullikuthashokk differentialrequirementformekpartner1indu145prostatecancercellmigration
AT parkelectar differentialrequirementformekpartner1indu145prostatecancercellmigration
AT mercantedonalde differentialrequirementformekpartner1indu145prostatecancercellmigration
AT catlingandrewd differentialrequirementformekpartner1indu145prostatecancercellmigration