ArticleMolecules (Basel, Switzerland)2022
WWOX Modulates ROS-Dependent Senescence in Bladder Cancer.
Article in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Exploring the Anticancer Potential of the Multistrain Probiotic FormulationAntioxidants (Basel, Switzerland) · 2025Article
- Review
- Molecular Mechanism of WWOX Inhibiting the Development of Esophageal Cancer by Inhibiting Hippo Signaling Pathway.Biochemical genetics · 2025Article
- Twenty-five years of WWOX insight in cancer: a treasure trove of knowledge.Functional & integrative genomics · 2025Review
- Inhibition of the FEN1-PBX1 axis elicits cellular senescence in breast cancer via the increased intracellular reactive oxygen species levels.Journal of translational medicine · 2025Article
- Novel Hydrogel-Mediated Lentiviral Gene Delivery via Intravesical Administration for Bladder Cancer Treatment.Pharmaceutics · 2025Article
- Senescence-related circRNA circHIF-1α is associated with pancreatic cancer progression.Cancer cell international · 2025Article
- Article
- The Molecular Mechanisms in Senescent Cells Induced by Natural Aging and Ionizing Radiation.Cells · 2024Review
- Zfra Overrides WWOX in Suppressing the Progression of Neurodegeneration.International journal of molecular sciences · 2024Review
- Induction of Senescence in Lung Cancer Cells by Qidongning Formula via the Transcription Factor EGR1.Integrative cancer therapiesArticle
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The tumor-suppressor gene, WW domain-containing oxidoreductase (WWOX), has been found to be lost in various types of cancers. ROS result as a tightly regulated signaling process for the induction of cell senescence. The aim of this study was to investigate the role of WWOX in the regulation of ROS and cell senescence, which is intriguing in terms of the possible mechanism of WWOX contributing to bladder cancer. In this study, we used the AY-27 rat bladder tumor cell line and F344 orthotopic bladder tumor models to reveal the pro-senescence effects of WWOX and the corresponding underlying mechanism in bladder cancer. WWOX-overexpressing lentivirus (LV-WWOX) remarkably stimulated cellular senescence, including increased senescence-associated secretory phenotype (SASP) formation, enlarged cellular morphology, and induced SA-β-Gal-positive staining. A further mechanism study revealed that the pro-senescence effect of LV-WWOX was dependent on increased intercellular reactive oxygen species (ROS) generation, which subsequently triggered p21/p27. Moreover, LV-WWOX significantly inhibited the tumor size by 30.49% in the F344/AY-27 rat orthotopic model (p < 0.05) by activating cellular senescence. The expression of p21 was significantly enhanced in the orthotopic bladder tumors under WWOX treatment. The orthotopic bladder tumors in the groups of rats verified the effect in vivo. Our study suggests that WWOX, an ROS-dependent senescence-induced gene, could be further studied for its therapeutic implications in bladder cancer.
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