This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kamai, T. Articles by Yoshida, K.-I. Search for Related Content PubMed PubMed Citation Articles by Kamai, T. Articles by Yoshida, K.-I.

Overexpression of RhoA, Rac1, and Cdc42 GTPases Is Associated with Progression in Testicular Cancer

¹ Department of Urology and ² Division of Molecular and Cell Biology, Dokkyo University School of Medicine, Tochigi, and Departments of ³ Urology and ⁴ Pathology, Tokyo Metropolitan Tama Geriatric Hospital, Tokyo, Japan

The Rho family of GTPases are involved in actin cytoskeleton organization and associated with carcinogenesis and progression of human cancers. We investigated the roles of Rho family GTPases, prototypes RhoA, Rac1, and Cdc42, and the major downstream targets of RhoA, ROCK-I, and ROCK-II in testicular cancer. We quantified protein expression in paired tumor and nontumor samples from surgical specimens from 57 consecutive patients with testicular germ cell tumors using Western blotting. Protein expression of RhoA, ROCK-I, ROCK-II, Rac1, and Cdc42 was significantly higher in tumor tissue than in nontumor tissue (P < 0.0001). Expression of protein for RhoA, ROCK-I, ROCK-II, Rac1, and Cdc42 was greater in tumors of higher stages than lower stages (P < 0.0001, P < 0.001, P < 0.001, P < 0.0001, P < 0.0001, respectively). Within stage II nonseminoma (31 patients), protein levels of RhoA, ROCK-I, ROCK-II, Rac1, and Cdc42 in the primary tumor were lower in the group of 24 patients with no evidence of disease after therapy compared with 7 patients with disease that was refractory/recurrent (P < 0.05). Rho family GTPases may be involved in the progression of testicular germ cell tumors.

This article has been cited by other articles:

				C. A. Marques, P. S. Hahnel, C. Wolfel, S. Thaler, C. Huber, M. Theobald, and M. Schuler An immune escape screen reveals Cdc42 as regulator of cancer susceptibility to lymphocyte-mediated tumor suppression Blood, February 1, 2008; 111(3): 1413 - 1419. [Abstract] [Full Text] [PDF]

				A. Schmandke, A. Schmandke, and S. M. Strittmatter ROCK and Rho: Biochemistry and Neuronal Functions of Rho-Associated Protein Kinases Neuroscientist, October 1, 2007; 13(5): 454 - 469. [Abstract] [PDF]

				C. Zhang, F. Zhou, N. Li, S. Shi, X. Feng, Z. Chen, J. Hang, B. Qiu, B. Li, S. Chang, et al. Overexpression of RhoE Has a Prognostic Value in Non Small Cell Lung Cancer Ann. Surg. Oncol., September 1, 2007; 14(9): 2628 - 2635. [Abstract] [Full Text] [PDF]

				V. Patel, H. M. Rosenfeldt, R. Lyons, J.-M. Servitja, X. R. Bustelo, M. Siroff, and J.S. Gutkind Persistent activation of Rac1 in squamous carcinomas of the head and neck: evidence for an EGFR/Vav2 signaling axis involved in cell invasion Carcinogenesis, June 1, 2007; 28(6): 1145 - 1152. [Abstract] [Full Text] [PDF]

				H. Lu, K. L. Knutson, E. Gad, and M. L. Disis The Tumor Antigen Repertoire Identified in Tumor-Bearing Neu Transgenic Mice Predicts Human Tumor Antigens Cancer Res., October 1, 2006; 66(19): 9754 - 9761. [Abstract] [Full Text] [PDF]