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Normal and cancer-related functions of the p160 steroid receptor co-activator (SRC) family

Journal

NATURE REVIEWS CANCER
Volume 9, Issue 9, Pages 615-630

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/nrc2695

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Funding

  1. US National Institutes of Health [R01DK058242, R01CA112403, R01CA119689, P01DK059820, R01HD07857, R01HD08818]
  2. National Institute of Diabetes and Digestive
  3. American Cancer Society Research Scholar Award [RSG-05-082-01]
  4. Susan Komen for the Cure Award [BCTR0707225]
  5. EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [R01HD008188, R01HD007857] Funding Source: NIH RePORTER
  6. NATIONAL CANCER INSTITUTE [R01CA119689, R01CA112403] Funding Source: NIH RePORTER
  7. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P01DK059820, R01DK058242] Funding Source: NIH RePORTER

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The three homologous members of the p160 SRC family (SRC1, SRC2 and SRC3) mediate the transcriptional functions of nuclear receptors and other transcription factors, and are the most studied of all the transcriptional co-activators. Recent work has indicated that the SRC genes are subject to amplification and overexpression in various human cancers. Some of the molecular mechanisms responsible for SRC overexpression, along with the mechanisms by which SRCs promote breast and prostate cancer cell proliferation and survival, have been identified, as have the specific contributions of individual SRC family members to spontaneous breast and prostate carcinogenesis in genetically manipulated mouse models. These studies have identified new challenges for cancer research and therapy.

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