Yuanyuan Fang1, Zhengtao Li, Xiuxia Wang, Shulan Zhang. 1. Department of Gynaecology and Obstetrics, Shengjing Hospital of China Medical University, [corrected] 36 Sanhao Street, Shenyang, 110004 Liaoning, People's Republic of China. fangyuanyuanpaper@yahoo.com.cn
Abstract
OBJECTIVE: δ-Catenin is found to be involved in the progression of several human cancers. However, its expression pattern and biological roles in human ovarian cancers are not clear. In this study, we examined the expression pattern of δ-catenin in 149 ovarian cancer specimens. We also depleted and overexpressed δ-catenin expression in ovarian cancer cell lines and investigated its role in cell proliferation and invasion. METHODS: δ-Catenin expression was analyzed in 149 archived ovarian cancer specimens using immunohistochemistry. siRNA knockdown and plasmid transfection were performed in SKOV3, SW626, and OVCAR3 cell lines. MTT, colony formation assay, soft agar colony assay, and matrigel invasion assay were carried out to assess the role of δ-catenin in cell proliferation and invasion. We also performed cell cycle analysis in δ-catenin depleted and overexpressed cells. In addition, we examined the level of several cell cycle-related molecules using Western blot. RESULTS: Of the 149 patients in the study, 104 (69.7 %) showed δ-catenin overexpression. δ-catenin overexpression positively correlated with advanced FIGO stage. δ-Catenin depletion in ovarian cancer cell lines inhibited ovarian cancer cell proliferation and invasion. Depletion of δ-catenin also blocked cell cycle progression and downregulated cyclin D1 expression in ovarian cancer cells. Overexpression of δ-catenin enhanced cell proliferation, invasion, and upregulated cyclinD1 expression. CONCLUSIONS: δ-Catenin is overexpressed in ovarian cancers and associated with advanced stage. Our data provide evidence that δ-catenin regulates the ovarian cancer cell proliferation, invasion, and cell cycle. δ-Catenin thus has potential as a therapeutic target.
OBJECTIVE: δ-Catenin is found to be involved in the progression of several humancancers. However, its expression pattern and biological roles in humanovarian cancers are not clear. In this study, we examined the expression pattern of δ-catenin in 149 ovarian cancer specimens. We also depleted and overexpressed δ-catenin expression in ovarian cancer cell lines and investigated its role in cell proliferation and invasion. METHODS: δ-Catenin expression was analyzed in 149 archived ovarian cancer specimens using immunohistochemistry. siRNA knockdown and plasmid transfection were performed in SKOV3, SW626, and OVCAR3 cell lines. MTT, colony formation assay, soft agar colony assay, and matrigel invasion assay were carried out to assess the role of δ-catenin in cell proliferation and invasion. We also performed cell cycle analysis in δ-catenin depleted and overexpressed cells. In addition, we examined the level of several cell cycle-related molecules using Western blot. RESULTS: Of the 149 patients in the study, 104 (69.7 %) showed δ-catenin overexpression. δ-catenin overexpression positively correlated with advanced FIGO stage. δ-Catenin depletion in ovarian cancer cell lines inhibited ovarian cancer cell proliferation and invasion. Depletion of δ-catenin also blocked cell cycle progression and downregulated cyclin D1 expression in ovarian cancer cells. Overexpression of δ-catenin enhanced cell proliferation, invasion, and upregulated cyclinD1 expression. CONCLUSIONS: δ-Catenin is overexpressed in ovarian cancers and associated with advanced stage. Our data provide evidence that δ-catenin regulates the ovarian cancer cell proliferation, invasion, and cell cycle. δ-Catenin thus has potential as a therapeutic target.
Authors: Fung Yu Huang; Pui Man Chiu; Kar Fai Tam; Yvonne K Y Kwok; Elizabeth T Lau; Mary H Y Tang; Tong Yow Ng; Vincent W S Liu; Annie N Y Cheung; Hextan Y S Ngan Journal: Gynecol Oncol Date: 2006-04-03 Impact factor: 5.482
Authors: Donald R Schwartz; Sharon L R Kardia; Kerby A Shedden; Rork Kuick; George Michailidis; Jeremy M G Taylor; David E Misek; Rong Wu; Yali Zhai; Danielle M Darrah; Heather Reed; Lora H Ellenson; Thomas J Giordano; Eric R Fearon; Samir M Hanash; Kathleen R Cho Journal: Cancer Res Date: 2002-08-15 Impact factor: 12.701