Zeng, YanAbdallah, AgustinLu, Jian-PingWang, TaoChen, Yan-HuaTerrian, David M.Kim, KwonseopLu, Qun2011-04-282011-05-172011-04-282011-05-172009-03-10Molecular Cancer; 8:19 p. 1-11http://hdl.handle.net/10342/3414Background: delta-Catenin is a unique member of delta-catenin/armadillo domain superfamily proteins and its primary expression is restricted to the brain. However, delta-catenin is upregulated in human prostatic adenocarcinomas, although the effects of delta-catenin overexpression in prostate cancer are unclear. We hypothesized that delta-catenin plays a direct role in prostate cancer progression by altering gene profiles of cell cycle regulation and cell survival. Results: We employed gene transfection and small interfering RNA to demonstrate that increased delta-catenin expression promoted, whereas its knockdown suppressed prostate cancer cell viability. delta-Catenin promoted prostate cancer cell colony formation in soft agar as well as tumor xenograft growth in nude mice. Deletion of either the amino-terminal or carboxyl-terminal sequences outside the armadillo domains abolished the tumor promoting effects of delta-catenin. Quantitative RT2 Profiler™ PCR Arrays demonstrated gene alterations involved in cell cycle and survival regulation. delta-Catenin overexpression upregulated cyclin D1 and cdc34, increased phosphorylated histone-H3, and promoted the entry of mitosis. In addition, delta-catenin overexpression resulted in increased expression of cell survival genes Bcl-2 and survivin while reducing the cell cycle inhibitor p21Cip1. Conclusion: Taken together, our studies suggest that at least one consequence of an increased expression of delta-catenin in human prostate cancer is the alteration of cell cycle and survival gene profiles, thereby promoting tumor progression. Originally published Molecular Cancer, Vol. 8, No. 19, Mar 2009en-USAuthor notified of opt-out rights by Cammie Jennings prior to upload of this article.CateninProstatic adenocarcinomasCell cycle--RegulationArticlePMC266027910.1186/1476-4598-8-19