期刊
CANCER CELL
卷 26, 期 1, 页码 92-105出版社
CELL PRESS
DOI: 10.1016/j.ccr.2014.04.027
关键词
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资金
- Charlotte Elizabeth Procter Fellowship
- Department of Defense [BC123187]
- Brewster Foundation
- Komen for the Cure
- NIH [R01CA134519]
- Breast Cancer Research foundation
- Transgenic/Knockout, Tissue Analytic Service and Flow Cytometry Shared Resources of the Cancer Institute of New Jersey [P30CA072720]
The Metadherin gene (MTDH) is prevalently amplified in breast cancer and associated with poor prognosis; however, its functional contribution to tunnorigenesis is poorly understood. Using mouse models representing different subtypes of breast cancer, we demonstrated that MTDH plays a critical role in mammary tumorigenesis by regulating oncogene-induced expansion and activities of tumor-initiating cells (TICs), whereas it is largely dispensable for normal development. Mechanistically, MTDH supports the survival of mammary epithelial cells under oncogenic/stress conditions by interacting with and stabilizing Staphylococcal nuclease domain-containing 1 (SND1). Silencing MTDH or SND1 individually or disrupting their interaction compromises tumorigenenic potential of TICs in vivo. This functional significance of MTDH-SND1 interaction is further supported by clinical analysis of human breast cancer samples.
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