Short report

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

Electa R Park^1,5 , Ashok K Pullikuth² , Evangeline M Bailey² , Donald E Mercante³ and Andrew D Catling^2,4

¹  Department of Biochemistry and Molecular Biology, LSU Health Sciences Center-New Orleans, LA, USA

²  Department of Pharmacology, LSU Health Sciences Center-New Orleans, LA, USA

³  Biostatistics Program, School of Public Health, LSU Health Sciences Center-New Orleans, LA, USA

⁴  Stanley S Scott Cancer Center, LSU Health Sciences Center-New Orleans, LA, USA

⁵  Laboratory of Integrin Signaling and Tumorigenesis, Van Andel Research Institute, Grand Rapids, MI, USA

author email corresponding author email

Cell Communication and Signaling 2009, 7:26doi:10.1186/1478-811X-7-26

Published:	23 November 2009

Abstract

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.