Related Experiment Video
Updated: May 9, 2026

Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
Published on: October 30, 2013
Steroid receptor coactivator-3 promotes bladder cancer through upregulation of CXCR4
Yu Zhang1, Ji-Hong Wang, Bin Liu
1Department of Urology, Shanghai Changning Center Hospital, Shanghai, China. ping_baoqu@126.com
Abstract:
The three homologous members of the p160 SRC family (SRC-1, SRC-2 and SRC-3) 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-3 gene is subject to amplification and overexpression in various human cancers. Some of the molecular mechanisms responsible for SRC overexpression, along with the mechanisms by which SRC-3 promotes breast and prostate cancer cell proliferation and survival, have been identified. However, the function of SRC-3 in bladder cancer remains poorly understood. In the present study, our results indicate that overexpression of SRC-3 promotes bladder cancer cell proliferation whereas knockdown of SRC-3 results in inhibition. At the molecular level, we further established that CXCR4 is a transcriptional target of SRC-3. Therefore, our study first identified that SRC-3 plays a critical role in the bladder cancer, which may be a target beneficial for its prevention and treatment.
Insights
SRC-3 (Steroid Receptor Coactivator-3) overexpression drives bladder cancer cell growth. Targeting SRC-3 and its downstream target CXCR4 may offer new bladder cancer prevention and treatment strategies.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- The p160 family of transcriptional coactivators, including SRC-3 (Steroid Receptor Coactivator-3), are crucial for nuclear receptor signaling.
- SRC-3 amplification and overexpression are implicated in various human cancers, promoting cell proliferation and survival.
- The specific role of SRC-3 in bladder cancer pathogenesis remains largely uncharacterized.
Purpose of the Study:
- To investigate the role of SRC-3 in bladder cancer.
- To identify molecular mechanisms by which SRC-3 influences bladder cancer progression.
- To explore SRC-3 as a potential therapeutic target for bladder cancer.
Main Methods:
- Utilized cell culture models of bladder cancer.
- Manipulated SRC-3 expression levels (overexpression and knockdown).
- Assessed the impact on cell proliferation and survival.
- Performed molecular analyses to identify transcriptional targets of SRC-3.
Main Results:
- SRC-3 overexpression significantly enhanced bladder cancer cell proliferation.
- Knockdown of SRC-3 expression inhibited bladder cancer cell proliferation.
- Identified CXCR4 as a direct transcriptional target of SRC-3 in bladder cancer cells.
Conclusions:
- SRC-3 plays a critical role in promoting bladder cancer cell proliferation.
- SRC-3's function in bladder cancer is mediated, in part, through the regulation of CXCR4.
- SRC-3 represents a promising molecular target for bladder cancer prevention and treatment strategies.
Related Concept Videos
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR activation may...
Mitogens and the Cell Cycle
Induced Pluripotent Stem Cells
Somatic cells are...
Abnormal Proliferation
