decorin suppresses prostate tumor growth through inhibition of epidermal growth factor and androgen receptor pathways

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ID: 212461
2009
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Abstract
Epidermal growth factor receptor (EGFR) and androgen receptor (AR) pathways play pivotal roles in prostate cancer progression. Therefore, agents with dual-targeting ability may have important therapeutic potential. Decorin, a proteoglycan present in the tumor microenvironment, is known to regulate matrix assembly, growth factor binding, and receptor tyrosine kinase activity. Here, we show that in prostate-specific PtenP-/- mice, a genetically defined, immune-competent mouse model of prostate cancer, systemic delivery of decorin inhibits tumor progression by targeting cell proliferation and survival pathways. Moreover, in human prostate cancer cells, we show that decorin specifically inhibits EGFR and AR phosphorylation and cross talk between these pathways. This prevents AR nuclear translocation and inhibits the production of prostate specific antigen. Further, the phosphatidylinositol-3 kinase (PI3K)/Akt cell survival pathway is suppressed leading to tumor cell apoptosis. Those findings highlight the effectiveness of decorin in the presence of a powerful genetic cancer risk and implicate decorin as a potential new agent for prostate cancer therapy by targeting EGFR/AR-PI3K-Akt pathways.
Reference Key
hu2009neoplasia:decorin Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Yunping Hu;Haiguo Sun;Rick T. Owens;Jiansheng Wu;Yong Q. Chen;Isabelle M. Berquin;Donna Perry;Joseph T. O'Flaherty;Iris J. Edwards
Journal ACS chemical neuroscience
Year 2009
DOI
10.1593/neo.09760
URL
http://www.sciencedirect.com/science/article/pii/S1476558609800079
Keywords
neoplasms Oncology including cancer and carcinogens tumors

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