The Role of StarD13 in Prostate Cancer Proliferation, Motility, and Invasion

Abstract

Prostate cancer is one of the most common tumors affecting males. Several risk factors predispose males to develop prostate cancer including age, ethnicity, and dietary habits. Even though it is easy to treat prostate cancer patients in the early stages, the danger of this disease resides in its being metastatic. Metastasis is a defining feature of invasive cancers, a process that includes invading the underlying matrix and migration of cells from the primary tumor to a distant location where they adhere and proliferate to form a new cancerous mass. Metastasis depends on the regulation of actin cytoskeleton dynamics established mainly by the family of Rho GTPases. Rho GTPases alternate between an active GTP-bound and inactive GDP-bound forms, which is accomplished by two classes of regulators, Rho GEFs that activate Rho GTPases by exchanging GDP with a GTP, and Rho GAPs that induce the hydrolysis of GTP into GDP rendering the Rho GTPases inactive. Among the Rho GAPs is StarD13, also called DLC2. In previous studies done at our lab, StarD13 is found to be a tumor suppressor in several tumor types like astrocytoma and breast cancer. In this study, we elaborated on the role of StarD13 in prostate cancer cellular proliferation, adhesion, invasion, and motility. We found that, in prostate cancer, StarD13 is underexpressed and it acts as a suppressor of tumor proliferation, adhesion, and invasion, however, StarD13 is a positive regulator of prostate cancer 2D motility.