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Carcinogenesis Advance Access originally published online on July 24, 2006
Carcinogenesis 2007 28(2):310-320; 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

Hyaluronan stimulates transformation of androgen-independent prostate cancer

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

Department of Cell and Neurobiology, Keck School of Medicine BMT-403, University of Southern California, 1333 San Pablo Street, Los Angeles, CA 90033, USA

*To whom correspondence should be addressed. Tel: +1 323 442 1856; Fax: +1 323 442 3466; Email: lins{at}usc.edu or sying{at}usc.edu

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 HA-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 CaP and enhance AI cell invasion and metastasis in human bone marrow endothelial layers. MicroRNA-based small hairpin RNA-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.

Abbreviations: AD, androgen-dependent; AI, androgen-independent; AR, androgen receptor; CaP, prostate cancer; ECM, extracellular matrix; EGFR, epidermal growth factor receptor; eIF4E, eukaryotic initiation factor 4E; HA, hyaluronan; HA-R, hyaluronan receptors; hBMEC, human bone marrow endothelial cell; HRCaP, hormone-refractory prostate cancer; IHC, immunohistochemical; LCM, laser-capture machine; miR, microRNA; MLC, myosin light chain; PBS, phosphate-buffered saline; PI3K, phosphatidylinositol-(3,4,5)P3 kinase; RNAi, RNA interference; RNA–PCR, RNA–polymerase cycling reaction; ROK, RhoA-activated protein kinase; shRNA, small hairpin RNA

Received April 27, 2006; revised July 10, 2006; accepted July 12, 2006.


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