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Carcinogenesis Advance Access published online on July 24, 2006
Carcinogenesis, doi:10.1093/carcin/bgl134
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received April 27, 2006
Revised July 10, 2006
Accepted July 12, 2006

CANCER BIOLOGY

Hyaluronan stimulates transformation of androgen-independent prostate cancer

Shi-Lung Lin 1 *, Donald Chang 1, and Shao-Yao Ying 1

1 Department of Cell and Neurobiology, Keck School of Medicine, University of Southern California, Los Angeles, California, USA

* To whom correspondence should be addressed.
Shi-Lung Lin, E-mail: lins{at}usc.edu


  Abstract

Interaction between extracellular matrices and cancer cell receptors frequently alters signal transduction pathways, leading to malignant transformation and metastasis. Hyaluronan (HA) is a tumor promoter and enhancer in transformation of androgen-independent (AI) prostate cancer (CaP); however, the signal transduction pathway involved in this mechanism remains unclear. We report here that HA-mediated CD168, a receptor for hyaluronan-mediated motility, and its downstream signal molecules, including ROK1, Gab-1, PI3K•p110{alpha} and eIF4E3, accelerate the progression of AI rather than androgen-dependent (AD) CaP and enhance AI cell invasion and metastasis in human bone marrow endothelial layers. MicroRNA (miR)-based shRNA-mediated suppression of ROK1 can reverse the malignant role of CD168 signaling in human AI CaP PC3 and DU145 cells. This differential activation of ROK-PI3K signaling in AI CaP cells may provide clues to shed light on some mechanisms of cancer relapse after androgen ablation. These findings reveal a novel signal transduction mechanism for matrix-mediated cancer transformation and metastasis in hormone-refractory CaP (HRCaP).

Keywords: prostate cancer; extracellular matrix (ECM); hyaluronan (HA); CD168 (RHAMM); rho kinase (ROK); PI3K; eIF4E; androgen-independent transformation; microRNA (miRNA); microarray; tissue array.
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