期刊
CANCER CELL
卷 16, 期 3, 页码 195-207出版社
CELL PRESS
DOI: 10.1016/j.ccr.2009.08.010
关键词
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资金
- Royal Golden Jubilee Program
- Thailand Research Fund
- National Institutes of Health [P30-CA 16672, RO1-CA109570, RO1-CA112567, PO1-CA099031, P50 CA116199]
- Department of Defense Center of Excellence [WB1XWH-06-2-0033]
- Synergistic Award [W81XWH-08-1-0712]
- Susan G. Komen Breast Cancer Foundation [KG091020]
ErbB2, a metastasis-promoting oncoprotein, is overexpressed in similar to 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 (I BC). We found that co-overexpression of 14-3-3 zeta in ErbB2-overexpressing DCIS conferred a higher risk of progression to IBC. ErbB2 and 14-3-3 zeta overexpression, respectively, increased cell migration and decreased cell adhesion, two prerequisites of tumor cell invasion. 14-3-3 zeta overexpression reduced cell adhesion by activating the TGF-beta/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 14-3-3 zeta had higher rates of metastatic recurrence and death than those whose tumors overexpressed only one.
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