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A more recent version of this article appeared on September 8, 2006
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M604376200v1
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Papers In Press, published online ahead of print June 20, 2006
J. Biol. Chem, 10.1074/jbc.M604376200
Submitted on May 8, 2006
Accepted on June 20, 2006

A role for the G12 family of heterotrimeric G-proteins in prostate cancer invasion

Patrick Kelly, Laura N. Stemmle, John F. Madden, Timothy A. Fields, Yehia Daaka, and Patrick J. Casey

Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710

Corresponding Author: casey006{at}mc.duke.edu

Many studies have suggested a role for the members of the G12 family of heterotrimeric G proteins (Galpha 12 and Galpha 13) in oncogenesis and tumor cell growth. However, few studies have examined G12 signaling in actual human cancers. In this study, we examined the role of G12 signaling in prostate cancer. We found that expression of the G12 proteins is significantly elevated in prostate cancer. Interestingly, expression of the activated forms of Galpha 12 or Galpha 13 in the PC3 and DU145 prostate cancer cell lines did not promote cancer cell growth. Instead, expression of the activated forms of Galpha 12 or Galpha 13 in these cell lines induced cell invasion through the activation of the RhoA family of G proteins. Furthermore, inhibition of G12 signaling by expression of the RGS domain of the p115-RhoGEF (p115-RGS) in the PC3 and DU145 cell lines did not reduce cancer cell growth. However, inhibition of G12 signaling with p115-RGS in these cell lines blocked thrombin- and thromboxane A2- stimulated cell invasion. These observations identify the G12 family proteins as important regulators of prostate cancer invasion and suggest these proteins may be targeted to limit invasion- and metastasis-induced prostate cancer patient mortality.


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