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...
Main Authors: | , , , , |
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Format: | Article |
Language: | English |
Published: |
BMC
2009-11-01
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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> |
first_indexed | 2024-12-10T19:09:44Z |
format | Article |
id | doaj.art-0b3c60a81bd54ba0807695393b84f7a6 |
institution | Directory Open Access Journal |
issn | 1478-811X |
language | English |
last_indexed | 2024-12-10T19:09:44Z |
publishDate | 2009-11-01 |
publisher | BMC |
record_format | Article |
series | Cell Communication and Signaling |
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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