期刊
MOLECULAR CANCER RESEARCH
卷 9, 期 10, 页码 1377-1384出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1541-7786.MCR-11-0198
关键词
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资金
- Novartis Research Foundation
- Marie-Curie reintegration grant
- European Research Council (ERC) [243211-PTPsBDC]
- Association of International Cancer Research (AICR)
- Krebsliga Beider Basel
- NIH [R37CA49132]
- Ontario Ministry of Long Term Care
- Princess Margaret Hospital Foundation
Protein-tyrosine phosphatase 1B (PTP1B), a well-established metabolic regulator, plays an important role in breast cancer. Using whole-body PTP1B knockout mice, recent studies have shown that PTP1B ablation delays HER2/Neu-induced mammary cancer. Whether PTP1B plays a cell-autonomous or a noncell-autonomous role in HER2/Neu-evoked tumorigenesis and whether it is involved in tumor maintenance was unknown. We generated mice expressing HER2/Neu and lacking PTP1B specifically in the mammary epithelium. We found that mammary-specific deletion of PTP1B delays the onset of HER2/Neu-evoked mammary tumors, establishing a cell autonomous role for PTP1B in such neoplasms. We also deleted PTP1B in established mouse mammary tumors or depleted PTP1B in human breast cancer cell lines grown as xenografts. PTP1B inhibition did not affect tumor growth in either model showing that neither epithelial nor stromal PTP1B is necessary for tumor maintenance. Taken together, our data show that despite the PTP1B contribution to tumor onset, it is not essential for tumor maintenance. This suggests that PTP1B inhibition could be effective in breast tumor prevention. Mol Cancer Res; 9(10); 1377-84. (C) 2011 AACR.
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