14-3-3zeta Cooperates with ErbB2 to promote ductal carcinoma in situ progression to invasive breast cancer by inducing epithelial-mesenchymal transition.
14-3-3zeta Cooperates with ErbB2 to promote ductal carcinoma in situ progression to invasive breast cancer by inducing epithelial-mesenchymal transition.
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DOI:
10.1016/j.ccr.2009.08.010
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发表时间:
2009-09-08
期刊:
影响因子:
50.3
通讯作者:
Yu D
中科院分区:
文献类型:
--
作者:
Lu J;Guo H;Treekitkarnmongkol W;Li P;Zhang J;Shi B;Ling C;Zhou X;Chen T;Chiao PJ;Feng X;Seewaldt VL;Muller WJ;Sahin A;Hung MC;Yu D
ErbB2, a metastasis-promoting oncoprotein, is overexpressed in ~25% of invasive/metastatic breast cancers, but in 50–60% of non-invasive 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 TGFβ/Smads pathway that led to ZFHX1B/SIP-1 upregulation, E-cadherin loss, and epithelial-mesenchymal transition (EMT). 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.
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DOI:
10.1016/j.biocel.2007.07.011
发表时间:
2007-01-01
影响因子:
4
作者:
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通讯作者:
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影响因子:
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作者:
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DOI:
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发表时间:
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影响因子:
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通讯作者:
Brugge, JS
影响因子:
6
作者:
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影响因子:
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作者:
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