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Prostate‐derived factor as a paracrine and autocrine factor for the proliferation of androgen receptor‐positive human prostate cancer cells
Author(s) -
Chen SiuJu,
Karan Dev,
Johansson Sonny L.,
Lin FenFen,
Zeckser Jeffrey,
Singh Ajay P.,
Batra Surinder K.,
Lin MingFong
Publication year - 2007
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.20551
Subject(s) - autocrine signalling , paracrine signalling , prostate cancer , prostate , clonogenic assay , cancer research , du145 , androgen receptor , cell growth , endocrinology , growth factor , biology , medicine , gene knockdown , receptor , cell culture , cancer , lncap , genetics
BACKGROUND The expression of prostate‐derived factor (PDF) is significantly elevated in human prostate tumors. We investigate the functional role and signaling of PDF in androgen receptor (AR)‐positive human prostate cancer cells. METHODS Transient or stable expression of PDF by cDNA transfection, antisense‐mediated gene silencing, media conditioned by PDF‐elevated cells, and antibody (Ab) neutralization were employed. RESULTS Elevated endogenous and exogenous expression of PDF and treatment of PDF‐enriched media were associated with increased proliferation and clonogenic growth of the cells. On the contrary, knockdown of PDF or addition of PDF neutralizing Ab resulted in diminished proliferation and reduced anchorage‐independent growth. Further, ERK1/2 and p90RSK, but not Smad2/3, were activated in PDF‐elevated cells as well as in cells treated with PDF‐enriched media, while inhibition of ERK1/2 decreased the growth of those cells. CONCLUSION PDF promotes AR‐positive prostate tumor progression through upregulating cell proliferation via ERK1/2 signal pathway. Prostate 67: 557–571, 2007. © 2007 Wiley‐Liss, Inc.