delta-Catenin promotes prostate cancer cell growth and progression by altering cell cycle and survival gene profiles

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dc.contributor.authorZeng, Yanen_US
dc.contributor.authorAbdallah, Agustinen_US
dc.contributor.authorLu, Jian-Pingen_US
dc.contributor.authorWang, Taoen_US
dc.contributor.authorChen, Yan-Huaen_US
dc.contributor.authorTerrian, David M.en_US
dc.contributor.authorKim, Kwonseopen_US
dc.contributor.authorLu, Qunen_US
dc.date.accessioned2011-04-28T18:11:38Zen_US
dc.date.accessioned2011-05-17T13:03:52Z
dc.date.available2011-04-28T18:11:38Zen_US
dc.date.available2011-05-17T13:03:52Z
dc.date.issued2009-03-10en_US
dc.description.abstractBackground: 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_US
dc.identifier.citationMolecular Cancer; 8:19 p. 1-11en_US
dc.identifier.doi10.1186/1476-4598-8-19
dc.identifier.pmidPMC2660279en_US
dc.identifier.urihttp://hdl.handle.net/10342/3414en_US
dc.language.isoen_USen_US
dc.publisherEast Carolina Universityen_US
dc.relation.urihttp://www.molecular-cancer.com/content/8/1/19en_US
dc.rightsAuthor notified of opt-out rights by Cammie Jennings prior to upload of this article.en_US
dc.subjectCateninen_US
dc.subjectProstatic adenocarcinomasen_US
dc.subjectCell cycle--Regulationen_US
dc.titledelta-Catenin promotes prostate cancer cell growth and progression by altering cell cycle and survival gene profilesen_US
dc.typeArticleen_US
ecu.journal.issue19
ecu.journal.nameMolecular Cancer
ecu.journal.pages1-11
ecu.journal.volume8

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