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Published on: September 5, 2018
SRC-3 has a role in cancer other than as a nuclear receptor coactivator
1Department of Surgical Oncology, First Affiliated Hospital, Medical School, Xi'an Jiaotong University, Xi'an, Shaanxi Province, 710061, P. R. China.
Abstract:
Steroid receptor coactivator-3 (SRC-3), also known as AIB1, is a member of the p160 steroid receptor coactivator family. Since SRC-3 was found to be amplified in breast cancer in 1997, the role of SRC-3 in cancer has been broadly investigated. SRC-3 initially was identified as a transcriptional coactivator for nuclear receptors such as the estrogen receptor (ER), involved in the proliferation of hormone-dependent cancers. However, increasing clinical evidence shows that dysregulation of SRC-3 expression in several human hormone-independent cancers is correlated with pathological factors and clinical prognosis. Recently, both in vivo and in vitro studies demonstrate that SRC-3 may influence a number of cancer cellular processes in several ways independent of nuclear receptor signaling. In addition, an SRC-3 transgenic mice model shows that SRC-3 induces tumors in several mouse tissues. These results indicate that the role of SRC-3 in cancer is not just as a nuclear receptor coactivator. The focus of this review is to examine possible SRC-3 roles in cancer, other than as a nuclear receptor coactivator.
Insights
Steroid receptor coactivator-3 (SRC-3) is crucial in hormone-dependent cancers. Emerging evidence reveals SRC-3 also drives hormone-independent cancers through novel mechanisms beyond its coactivator role.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Steroid receptor coactivator-3 (SRC-3), also known as AIB1, is part of the p160 family.
- SRC-3 amplification in breast cancer (1997) spurred extensive research into its oncogenic roles.
- Initially recognized for coactivating nuclear receptors like estrogen receptor (ER) in hormone-dependent cancers.
Purpose of the Study:
- To review the multifaceted roles of SRC-3 in cancer.
- To explore SRC-3 functions beyond its established role as a nuclear receptor coactivator.
- To examine SRC-3's involvement in hormone-independent cancers.
Main Methods:
- Literature review of in vivo and in vitro studies.
- Analysis of clinical evidence on SRC-3 expression and cancer pathology.
- Examination of data from SRC-3 transgenic mouse models.
Main Results:
- SRC-3 dysregulation correlates with poor prognosis in hormone-independent cancers.
- In vivo and in vitro studies show SRC-3 influences cancer processes independently of nuclear receptors.
- SRC-3 transgenic models demonstrate its potential to induce tumors across various tissues.
Conclusions:
- SRC-3's role in cancer extends beyond nuclear receptor coactivation.
- SRC-3 is implicated in the progression of hormone-independent cancers.
- Further investigation into non-coactivator functions of SRC-3 is warranted for therapeutic strategies.
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