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Updated: Jun 20, 2026

Reverse Yeast Two-hybrid System to Identify Mammalian Nuclear Receptor Residues that Interact with Ligands and/or Antagonists
Published on: November 15, 2013
Normal and cancer-related functions of the p160 steroid receptor co-activator (SRC) family
Jianming Xu1, Ray-Chang Wu, Bert W O'Malley
1Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA. jxu@bcm.tmc.edu
Abstract:
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 SRCgenes 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.
Insights
SRC co-activators are crucial for nuclear receptor function and are overexpressed in cancers. Research is uncovering mechanisms of SRC overexpression and their role in promoting cancer cell survival and proliferation.
Area of Science:
- Molecular Biology
- Genetics
- Oncology
Background:
- SRC1, SRC2, and SRC3 are p160 family members and transcriptional co-activators.
- SRC genes are amplified and overexpressed in human cancers.
- SRC co-activators mediate nuclear receptor and transcription factor functions.
Purpose of the Study:
- To investigate the molecular mechanisms of SRC overexpression in cancer.
- To elucidate how SRCs promote cancer cell proliferation and survival.
- To understand the specific roles of individual SRC family members in carcinogenesis.
Main Methods:
- Analysis of molecular mechanisms driving SRC overexpression.
- Studies on SRC-mediated promotion of cancer cell proliferation and survival.
- Utilizing genetically manipulated mouse models to study SRC contributions to spontaneous carcinogenesis.
Main Results:
- Identified molecular mechanisms underlying SRC overexpression.
- Elucidated SRC roles in promoting breast and prostate cancer cell proliferation and survival.
- Determined specific contributions of SRC1, SRC2, and SRC3 to spontaneous carcinogenesis in mouse models.
Conclusions:
- SRC family members play significant roles in cancer development and progression.
- Understanding SRC mechanisms presents new challenges and opportunities for cancer therapy.
- Further research into SRC co-activators is critical for advancing cancer treatment strategies.
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