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Salinomycin Exerts Anticancer Effects on PC-3 Cells and PC-3-Derived Cancer Stem Cells In Vitro and In Vivo
Yunsheng Zhang1, Luogen Liu1, Fang Li2
1Clinical Research Institute, The Second Affiliated Hospital, University of South China, Hengyang 421001, China.
Abstract:
Salinomycin is an antibiotic isolated from Streptomyces albus that selectively kills cancer stem cells (CSCs). However, the antitumor mechanism of salinomycin is unclear. This study investigated the chemotherapeutic efficacy of salinomycin in human prostate cancer PC-3 cells. We found that cytotoxicity of salinomycin to PC-3 cells was stronger than to nonmalignant prostate cell RWPE-1, and exposure to salinomycin induced G2/M phage arrest and apoptosis of PC-3 cells. A mechanistic study found salinomycin suppressed Wnt/β-catenin pathway to induce apoptosis of PC-3 cells. An in vivo experiment confirmed that salinomycin suppressed tumorigenesis in a NOD/SCID mice xenograft model generated from implanted PC-3 cells by inhibiting the Wnt/β-catenin pathway, since the total β-catenin protein level was reduced and the downstream target c-Myc level was significantly downregulated. We also showed that salinomycin, but not paclitaxel, triggered more apoptosis in aldehyde dehydrogenase- (ALDH-) positive PC-3 cells, which were considered as the prostate cancer stem cells, suggesting that salinomycin may be a promising chemotherapeutic to target CSCs. In conclusion, this study suggests that salinomycin reduces resistance and relapse of prostate tumor by killing cancer cells as well as CSCs.
Insights
Salinomycin effectively targets prostate cancer stem cells (CSCs) by inducing apoptosis and suppressing the Wnt/β-catenin pathway. This antibiotic shows promise in reducing tumor resistance and relapse, offering a new therapeutic strategy.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Salinomycin, an antibiotic from *Streptomyces albus*, selectively targets cancer stem cells (CSCs).
- The precise antitumor mechanism of salinomycin remains incompletely understood.
- Prostate cancer exhibits resistance and relapse, often linked to CSC populations.
Purpose of the Study:
- To investigate the chemotherapeutic efficacy and mechanism of salinomycin in human prostate cancer PC-3 cells.
- To evaluate salinomycin's potential to target prostate cancer stem cells (CSCs).
- To elucidate salinomycin's effect on the Wnt/β-catenin pathway in prostate cancer.
Main Methods:
- Cytotoxicity assays comparing salinomycin effects on PC-3 cells versus RWPE-1 cells.
- Cell cycle analysis (G2/M phase arrest) and apoptosis assays.
- Western blot analysis to assess Wnt/β-catenin pathway components (β-catenin, c-Myc) and in vivo xenograft studies in NOD/SCID mice.
Main Results:
- Salinomycin exhibited greater cytotoxicity towards PC-3 cells than RWPE-1 cells, inducing G2/M phase arrest and apoptosis.
- Salinomycin suppressed the Wnt/β-catenin pathway, reducing β-catenin and c-Myc levels, thereby inducing apoptosis.
- Salinomycin triggered more apoptosis in aldehyde dehydrogenase- (ALDH-) positive PC-3 cells (prostate CSCs) compared to paclitaxel.
Conclusions:
- Salinomycin demonstrates significant antitumor efficacy against prostate cancer by inhibiting the Wnt/β-catenin pathway and inducing apoptosis in both cancer cells and CSCs.
- Salinomycin's ability to target CSCs suggests its potential to overcome treatment resistance and reduce tumor relapse.
- Salinomycin represents a promising chemotherapeutic agent for targeting prostate cancer, including its stem cell population.
