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The effect of PKD1 expression on prostate cancer cell proliferation was analyzed in AR transfected DU145 or LNCaP Daptomycin in the absence or presence of PKD1 or PKD1-kinase mutant (K628W) expression plasmids. As shown in Fig. 4C, in the presence of DHT (10 nM), there was a 3-fold increase of cell proliferation in both cell lines. This effect was abolished by incubating with the AR antagonist Casodex (10 μM) indicating that the growth promoting effect of DHT on PC cells is specifically mediated through AR. While expression of PKD1 alone could inhibit cell proliferation, Co-expression of PKD1 or kinase dead PKD1 (K628W) with AR could abolish the ligand-dependent AR mediated growth demonstrating that PKD1 inhibits AR mediated cell proliferation, which may be independent of PKD1-kinase activity.
Discussion
In conclusion, the current study demonstrates that PKD1 is a novel interacting protein of AR in PCa cells. Because both PKD1 and AR are dysregulated in prostate cancer, PKD1–AR interaction provides us a novel signaling pathway worth exploring further to understand prostate cancer progression. Further examination and correlation in the expression of PKD1 and AR in normal and different Gleason grades and stages of PCa tissues can provide novel insights into this newly discovered PKD1–AR signaling pathway in prostate cancer.