Exploring the Anticancer Potential of the Multistrain Probiotic Formulation OxxySlab in Bladder Cancer Cell Lines.
- 2025-10-26
- Antioxidants (Basel, Switzerland) 14(11)
- Valeria Ciummo
- Alessia Ciafarone
- Serena Altamura
- Francesca Lombardi
- Marcella Reale
- Maria Grazia Cifone
- Benedetta Cinque
- Paola Palumbo
- PubMed: 41300439
- DOI: 10.3390/antiox14111282
Study Design
- Population
- two BC cell lines (T24 and 5637) and a non-tumorigenic urothelial cell line (SV-HUC1)
- Methods
- <i>OxxySlab</i> lysate dose-dependently inhibited BC cell proliferation, clonogenicity, and migration; mechanistically, the treatment suppressed epithelial-mesenchymal transition (EMT), induced senescence, and disrupted redox homeostasis in malignant cells. Co-treatment with vitamin C attenuated ROS accumulation and senescence.
Bladder cancer (BC), particularly its muscle-invasive subtype (MIBC), remains a clinical challenge due to high recurrence and limited therapeutic options. Emerging evidence suggests that probiotics may offer selective anticancer effects while preserving healthy tissue. In this study, we evaluated the antitumor potential of OxxySlab, a multistrain probiotic formulation, in two BC cell lines (T24 and 5637) and a non-tumorigenic urothelial cell line (SV-HUC1). OxxySlab lysate dose-dependently inhibited BC cell proliferation, clonogenicity, and migration, while sparing normal cells. Mechanistically, the treatment suppressed epithelial-mesenchymal transition (EMT), induced senescence, and disrupted redox homeostasis in malignant cells. These effects were associated with the induction of oxidative stress and impaired antioxidant defenses. Co-treatment with vitamin C attenuated ROS accumulation and senescence, implicating oxidative stress as a key mediator. Notably, SV-HUC1 cells retained viability and phenotype, confirming the formulation's selectivity. Overall, these findings support OxxySlab as a promising adjunctive strategy in BC therapy, capable of reducing tumor aggressiveness through redox-mediated senescence and EMT inhibition without harming normal urothelial cells.
Research Insights
Mechanistically, the treatment suppressed epithelial-mesenchymal transition (EMT), induced senescence, and disrupted redox homeostasis in malignant cells.
- Effect
- Beneficial
- Effect size
- Moderate
Notably, SV-HUC1 cells retained viability and phenotype, confirming the formulation's selectivity.
- Effect
- Beneficial
- Effect size
- Small