Prostate-derived factor as a paracrine and autocrine factor for the proliferation of androgen receptor-positive human prostate cancer cells

Siu Ju Chen, Dev Karan, Sonny L. Johansson, Fen Fen Lin, Jeffrey Zeckser, Ajay P. Singh, Surinder Kumar Batra, Ming-Fong Lin

Research output: Contribution to journalArticle

55 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)557-571
Number of pages15
JournalProstate
Volume67
Issue number5
DOIs
StatePublished - Apr 1 2007

Fingerprint

Prostate
Prostatic Neoplasms
human AR protein
Growth
MAP Kinase Signaling System
Androgen Receptors
Gene Silencing
Conditioned Culture Medium
Neutralizing Antibodies
Transfection
Signal Transduction
Neoplasms
Complementary DNA
Cell Proliferation
Antibodies

Keywords

  • Prostate tumorigenesis
  • Prostate-derived factor
  • TGF-beta signaling

ASJC Scopus subject areas

  • Oncology
  • Urology

Cite this

Prostate-derived factor as a paracrine and autocrine factor for the proliferation of androgen receptor-positive human prostate cancer cells. / Chen, Siu Ju; Karan, Dev; Johansson, Sonny L.; Lin, Fen Fen; Zeckser, Jeffrey; Singh, Ajay P.; Batra, Surinder Kumar; Lin, Ming-Fong.

In: Prostate, Vol. 67, No. 5, 01.04.2007, p. 557-571.

Research output: Contribution to journalArticle

Chen, Siu Ju ; Karan, Dev ; Johansson, Sonny L. ; Lin, Fen Fen ; Zeckser, Jeffrey ; Singh, Ajay P. ; Batra, Surinder Kumar ; Lin, Ming-Fong. / Prostate-derived factor as a paracrine and autocrine factor for the proliferation of androgen receptor-positive human prostate cancer cells. In: Prostate. 2007 ; Vol. 67, No. 5. pp. 557-571.
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abstract = "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.",
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AU - Chen, Siu Ju

AU - Karan, Dev

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AU - Lin, Fen Fen

AU - Zeckser, Jeffrey

AU - Singh, Ajay P.

AU - Batra, Surinder Kumar

AU - Lin, Ming-Fong

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N2 - 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.

AB - 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.

KW - Prostate tumorigenesis

KW - Prostate-derived factor

KW - TGF-beta signaling

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