期刊
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
卷 8, 期 4, 页码 470-485出版社
IVYSPRING INT PUBL
DOI: 10.7150/ijbs.4125
关键词
nuclear receptor; coactivator; SRC-1; transcription; development; cancer
资金
- Cancer Prevention and Research Institute of Texas [RP101251-P4]
- National Institutes of Health [R01 CA112403, R01 DK058242]
- Department of Defense [PC102004]
- Science Foundation Ireland [B1853]
- Health Research Board, Ireland [PHD/2007/11]
- NATIONAL CANCER INSTITUTE [R01CA112403] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK058242] Funding Source: NIH RePORTER
In 1995, the steroid receptor coactivator-1 (SRC-1) was identified as the first authentic steroid receptor coactivator. Since then, the SRC proteins have remained at the epicenter of coregulator biology, molecular endocrinology and endocrine-related cancer. Cumulative works on SRC-1 have shown that it is primarily a nuclear receptor coregulator and functions to construct highly specific enzymatic protein complexes which can execute efficient and successful transcriptional activation of designated target genes. The versatile nature of SRC-1 enables it to respond to steroid dependent and steroid independent stimulation, allowing it to bind across many families of transcription factors to orchestrate and regulate complex physiological reactions. This review highlights the multiple functions of SRC-1 in the development and maintenance of normal tissue functions as well as its major role in mediating hormone receptor responsiveness. Insights from genetically manipulated mouse models and clinical data suggest SRC-1 is significantly overexpressed in many cancers, in particular, cancers of the reproductive tissues. SRC-1 has been associated with cellular proliferation and tumor growth but its major tumorigenic contributions are promotion and execution of breast cancer metastasis and mediation of resistance to endocrine therapies. The ability of SRC-1 to coordinate multiple signaling pathways makes it an important player in tumor cells' escape of targeted therapy.
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