EPLIN is a negative regulator of prostate cancer growth and invasion - Abstract

Metastasis and Angiogenesis Research Group, Cardiff University School of Medicine, Cardiff, United Kingdom.


We investigated the importance of EPLIN, a cytoskeletal associated protein implicated in cancer, in clinical prostate cancer and its role in the PC-3 prostate cancer cell line (ATCC™).

Full-length human EPLIN cDNA was cloned into a pEF6 expression vector and used to transfect the PC-3 human prostate cancer cell line. Cells over expressing EPLIN were termed PC-3(EPLIN EXP) while wild-type and empty pEF6 vector control cells were designated PC-3(WT) and PC-3(pEF6), respectively. The in vitro and in vivo impact of EPLIN on PC-3 cells was examined using a number of model assays.

EPLIN over expression in PC-3 cells resulted in a decrease in the growth rate of this cell line (mean ± SD 0.6 ± 0.17 for PC-3(pEF6) cells vs 0.33 ± 0.01 for PC-3(EPLIN EXP) cells, p < 0.01). PC-3(EPLIN EXP) cells were significantly less able to adhere to extracellular matrix than control cells (mean 61.0 ± 12.4 vs 102.8 ± 20.7, p = 0.028). Immunofluorescence staining showed an increased staining profile for paxillin in PC-3(EPLIN EXP) cells compared to wild-type cells.

EPLIN over expression in the PC-3 cell line resulted in decreased in vivo and in vitro growth potential together with decreased cell invasiveness and ability to adhere to extracellular matrix, and enhanced paxillin staining. This further highlights the importance of EPLIN in regulating prostate cancer cell growth and aggressiveness, and suggests a possible connection between EPLIN and paxillin.

Written by:
Sanders AJ, Martin TA, Ye L, Mason MD, Jiang WG.   Are you the author?

Reference: J Urol. 2011 May 18. Epub ahead of print.
doi: 10.1016/j.juro.2011.03.038

PubMed Abstract
PMID: 21600601

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