Abstract
Abstract Rho family proteins are prominent members of the well-known Ras superfamily and are deeply involved in almost all the malignant behaviors of cancer. As Small GTPases, Rho proteins can cycle between active GTP-bound state and GDP-bound state by regulating of GEFs, GAP and GDI. RhoE is a unique member of Rho family proteins that can bind but do not hydrolyze GTP, thus remain constitutively active upon expression without the need of regulation by the GTP/GDP conformational changes of other Rho GTPases. Previous studies have shown that RhoE may play a role opposite that of RhoA in regulating cell proliferation. Here, for the first time, we systematically investigate the expression patterns of RhoE by systemic immunocytochemistry analysis of 74, 32, 62, and 34 gastric, colorectal, lung, and breast carcinomas, respectively, and found that RhoE protein level was significantly decreased in most cancer cases compared with that of adjacent normal tissues. RhoE expression also appeared to inversely correlate with the clinical grade of gastric, colorectal, lung cancer tissues. Increasing RhoE expression in MKN45, SW480, HepG2 and SPCA1 cancer cell lines that have relatively low level of endogenous RhoE could markedly inhibit proliferation, migration and invasion activities and induced apoptosis of the cancer cells. Interestingly, p53 transcription activity was reduced in these RhoE under-expressed cancer cells that contain p53 mutations, and increasing p53 activity significantly increased RhoE expression in the cells. Significantly, p53 transcription activity, measured by the p53-responsive p21Cip1, MDM2, and GADD45 expressions, paralleled RhoE expression in gastric cancer tissues. Thus, RhoE may participate in human cancer progression as a candidate tumor suppressor under the regulation by p53. This work also enriches our knowledge in the role of small G protein network in cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2146. doi:1538-7445.AM2012-2146
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