14-3-3z Cooperates with ErbB2 to Promote Ductal Carcinoma In Situ Progression to Invasive Breast Cancer by Inducing Epithelial-Mesenchymal Transition

中國醫藥大學機構典藏 China Medical University Repository, Taiwan > 醫學院 > 癌症生物學研究所 > 期刊論文 > Item 310903500/31229

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題名:	14-3-3z Cooperates with ErbB2 to Promote Ductal Carcinoma In Situ Progression to Invasive Breast Cancer by Inducing Epithelial-Mesenchymal Transition
作者:	(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)*
貢獻者:	醫學院癌症生物學研究所;中國附醫院長室
關鍵詞:	CELLCYCLE
日期:	2009
上傳時間:	2010-09-27 15:48:20 (UTC+8)
摘要:	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.
關聯:	CANCER CELL 16(3):195-207
顯示於類別:	[癌症生物學研究所] 期刊論文

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