SRC-3 is required for prostate cancer cell proliferation and survival
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Updated: Aug 16, 2026
A Rapid Filter Insert-based 3D Culture System for Primary Prostate Cell Differentiation
Published on: February 13, 2017
Hai-Jun Zhou1, Jun Yan, Weiping Luo
1Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA.
Abstract:
Prostate cancer is the most common cancer in men in America. Currently, steroid receptor coactivators have been proposed to mediate the development and progression of prostate cancer, at times in a steroid-independent manner. Steroid receptor coactivator-3 (SRC-3, p/CIP, AIB1, ACTR, RAC3, and TRAM-1) is a member of the p160 family of coactivators for nuclear hormone receptors including the androgen receptor. SRC-3 is frequently amplified or overexpressed in a number of cancers. However, the role of SRC-3 in cancer cell proliferation and survival is still poorly understood. In this study, we show that SRC-3 is overexpressed in prostate cancer patients and its overexpression correlates with prostate cancer proliferation and is inversely correlated with apoptosis. Consistent with patient data, we have observed that reduction of SRC-3 expression by small interfering RNA decreases proliferation, delays the G1-S transition, and increases cell apoptosis of different prostate cancer cell lines. Furthermore, with decreased SRC-3 expression, proliferating cell nuclear antigen and Bcl-2 expression, as well as bromodeoxyuridine incorporation in prostate cancer cells are reduced. Finally, knockdown of SRC-3 with inducible short hairpin RNA expression in prostate cancer cells decreased tumor growth in nude mice. Taken together, these findings indicate that SRC-3 is an important regulator of prostate cancer proliferation and survival.
Insights
Steroid receptor coactivator-3 (SRC-3) is overexpressed in prostate cancer, driving tumor growth and survival. Reducing SRC-3 levels inhibits proliferation and induces apoptosis, offering a potential therapeutic target for prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Prostate cancer is a leading cancer in men.
- Steroid receptor coactivators, including SRC-3, are implicated in prostate cancer development.
- The precise role of SRC-3 in cancer cell proliferation and survival requires further elucidation.
Purpose of the Study:
- To investigate the role of Steroid Receptor Coactivator-3 (SRC-3) in prostate cancer proliferation and survival.
- To determine the correlation between SRC-3 expression and clinical outcomes in prostate cancer patients.
Main Methods:
- Analysis of SRC-3 expression in prostate cancer patient samples.
- Utilized small interfering RNA (siRNA) to reduce SRC-3 expression in prostate cancer cell lines.
- Employed inducible short hairpin RNA (shRNA) to assess the impact of SRC-3 knockdown on tumor growth in vivo.
- Measured cell proliferation, cell cycle progression (G1-S transition), and apoptosis.
Main Results:
- SRC-3 is overexpressed in prostate cancer, correlating with increased proliferation and decreased apoptosis.
- Reduction of SRC-3 expression via siRNA decreased proliferation, delayed G1-S transition, and increased apoptosis in prostate cancer cell lines.
- Decreased SRC-3 expression led to reduced levels of proliferating cell nuclear antigen (PCNA) and Bcl-2.
- Knockdown of SRC-3 using inducible shRNA significantly inhibited tumor growth in nude mice.
Conclusions:
- SRC-3 is a significant regulator of prostate cancer cell proliferation and survival.
- Targeting SRC-3 may represent a viable therapeutic strategy for managing prostate cancer growth.
