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A New Technique for Treating Low-risk Prostate Cancer—Super Active Surveillance
Published on: November 7, 2025
Antimony enhances c-Myc stability in prostate cancer via activating CtBP2-ROCK1 signaling pathway
Changwen Zhang1, Chao Lu1, Zhen Wang1
1Department of Urology, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin 300211, China.
Abstract:
Antimony, one of the heavier pnictogens, is widely used in industry, and its toxicity has become a major concern. Although previous studies suggested that antimony might be a tumorigenic risk factor in several cancers, the molecular basis underlying antimony-mediated transformation remains unclear. Our results showed that the serum concentration of antimony was higher in prostate cancer specimens relative to that of benign prostate tissues, and this high serum concentration of antimony was closely associated with poorer outcome in prostate cancer patients. Additionally, we demonstrated that antimony could promote prostate cancer cell growth in vitro and in vivo. In order to gain insight into the potential mechanisms, we examined the effects of antimony exposure on downstream signaling that could contribute to tumor development. We found that low-dose antimony could regulate the expression of Ctbp2 by binding and regulating the activity of its MRE domain. Meanwhile, CtBP2 could transcriptionally regulate the expression of RhoC, which is a member of the RhoGTPase family. Subsequently, the kinase activity of ROCK1 is increased, which promotes the stability of oncogene c-Myc. Overall, our study demonstrated that antimony could enhance c-Myc protein stability and promote prostate cancer cell proliferation through activating CtBP2-ROCK1 signaling pathway. These findings also substantially highlighted the potential of targeting molecules within antimony induced CtBP2-c-Myc signaling pathway as a promising therapeutic approach for the treatment of prostate cancer.
Insights
Antimony exposure is linked to higher prostate cancer risk and poorer outcomes. This study reveals antimony promotes cancer cell growth by stabilizing c-Myc via the CtBP2-ROCK1 pathway, suggesting a new therapeutic target.
Area of Science:
- Environmental Health
- Oncology
- Molecular Biology
Background:
- Antimony is an industrial element with increasing toxicity concerns.
- Previous research suggests antimony as a potential tumorigenic risk factor, but molecular mechanisms are unclear.
- Prostate cancer remains a significant health concern globally.
Purpose of the Study:
- To investigate the association between serum antimony levels and prostate cancer.
- To elucidate the molecular mechanisms by which antimony promotes prostate cancer progression.
- To identify potential therapeutic targets within the antimony-induced signaling pathway.
Main Methods:
- Serum antimony levels were measured in prostate cancer patients and healthy controls.
- In vitro and in vivo models were used to assess antimony's effect on prostate cancer cell growth.
- Molecular signaling pathways, including CtBP2, RhoC, ROCK1, and c-Myc, were analyzed following antimony exposure.
Main Results:
- Serum antimony concentrations were significantly higher in prostate cancer tissues compared to benign tissues.
- Elevated serum antimony levels correlated with poorer patient outcomes.
- Antimony exposure promoted prostate cancer cell proliferation both in vitro and in vivo.
- Antimony was found to enhance c-Myc protein stability by activating the CtBP2-ROCK1 signaling pathway.
Conclusions:
- Antimony exposure is associated with increased prostate cancer risk and progression.
- The CtBP2-ROCK1-c-Myc signaling pathway is a key mediator of antimony's oncogenic effects in prostate cancer.
- Targeting the CtBP2-c-Myc pathway presents a potential therapeutic strategy for managing antimony-related prostate cancer.
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