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Please use this identifier to cite or link to this item: http://ir.cmu.edu.tw/ir/handle/310903500/31229

Title: 14-3-3z Cooperates with ErbB2 to Promote Ductal Carcinoma In Situ Progression to Invasive Breast Cancer by Inducing Epithelial-Mesenchymal Transition
Authors: (Lu, J,);(Guo, H);(Treekitkarnmongkol, W);(Li, P.);(Zhang, J);(Shi, B);(Ling C);(Zhou, X);(Chen, T);(Chiao, P);(Feng X);(Seewaldt, V);(Muller, W);(Sahin, A);洪明奇(Mien-Chie Hung);(Yu, D)*
Contributors: 醫學院癌症生物學研究所;中國附醫院長室
Keywords: CELLCYCLE
Date: 2009
Issue Date: 2010-09-27 15:48:20 (UTC+8)
Abstract: ErbB2, a metastasis-promoting oncoprotein, is overexpressed in 25% of invasive/metastatic breast cancers, but in 50%–60% of noninvasive ductal carcinomas in situ (DCIS). It has been puzzling how a subset of ErbB2-overexpressing DCIS develops into invasive breast cancer (IBC). We found that co-overexpression of 14-3-3ζ in ErbB2-overexpressing DCIS conferred a higher risk of progression to IBC. ErbB2 and 14-3-3ζ overexpression, respectively, increased cell migration and decreased cell adhesion, two prerequisites of tumor cell invasion. 14-3-3ζ overexpression reduced cell adhesion by activating the TGF-β/Smads pathway that led to ZFHX1B/SIP-1 upregulation, E-cadherin loss, and epithelial-mesenchymal transition. Importantly, patients whose breast tumors overexpressed both ErbB2 and 14-3-3ζ had higher rates of metastatic recurrence and death than those whose tumors overexpressed only one.
Relation: CANCER CELL 16(3):195-207
Appears in Collections:[癌症生物學研究所] 期刊論文

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