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

被引:47
|
作者
Zeng, Yan [1 ]
Abdallah, Agustin [1 ]
Lu, Jian-Ping [1 ]
Wang, Tao [1 ,3 ]
Chen, Yan-Hua [1 ,2 ]
Terrian, David M. [1 ,2 ]
Kim, Kwonseop [1 ,4 ]
Lu, Qun [1 ,2 ]
机构
[1] E Carolina Univ, Brody Sch Med, Dept Anat & Cell Biol, Greenville, NC 27858 USA
[2] E Carolina Univ, Brody Sch Med, Leo Jenkins Canc Ctr, Greenville, NC 27858 USA
[3] Beijing Capital Med Univ, Dept Surg, Beijing, Peoples R China
[4] Chonnam Natl Univ, Coll Pharm, Kwangju, South Korea
关键词
ARMADILLO PROTEIN; E-CADHERIN; EXPRESSION; MORPHOGENESIS; REDISTRIBUTION; IDENTIFICATION; PROLIFERATION; COMPLEX; KINASE; MEMBER;
D O I
10.1186/1476-4598-8-19
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: delta-Catenin is a unique member of beta-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 (TM) 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 p21(Cip1). 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.
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页数:11
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