ArticleInternational journal of molecular sciences2019
Loss of Tumor Suppressor CYLD Expression Triggers Cisplatin Resistance in Oral Squamous Cell Carcinoma.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- The role of e3 ubiquitin ligases and deubiquitinating enzymes in hepatocellular carcinoma.Cell biology and toxicology · 2026Review
- lncRNACancers · 2026Article
- Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025Review
- Evolving role of deubiquitinating enzymes in oral cancer (Review).Oncology letters · 2025Review
- A two-decade bibliometric analysis of drug resistance in oral cancer research: patterns, trends, and future directions.Discover oncology · 2025Article
- Suppression of CYLD by HER3 confers ovarian cancer platinum resistance via inhibiting apoptosis and by inducing drug efflux.Experimental hematology & oncology · 2025Article
- Deubiquitinases and Cancer.Journal of pharmacy & bioallied sciences · 2024Review
- Comparison of mutation landscapes of pretreatment versus recurrent squamous cell carcinoma of the oral cavity: The possible mechanism of resistance to standard treatment.Cancer reports (Hoboken, N.J.) · 2024Article
- CYLD induces high oxidative stress and DNA damage through class I HDACs to promote radiosensitivity in nasopharyngeal carcinoma.Cell death & disease · 2024Article
- Gastrodin overcomes chemoresistance via inhibiting Skp2-mediated glycolysis.Cell death discovery · 2023Article
- HPV Enhances HNSCC Chemosensitization by Inhibiting SERPINB3 Expression to Disrupt the Fanconi Anemia Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Potential use of EGFR-targeted molecular therapies for tumor suppressor CYLD-negative and poor prognosis oral squamous cell carcinoma with chemoresistance.Cancer cell international · 2022Article
- Cisplatin Resistance: Genetic and Epigenetic Factors Involved.Biomolecules · 2022Review
- MicroRNA-485-5p targets keratin 17 to regulate oral cancer stemness and chemoresistance via the integrin/FAK/Src/ERK/β-catenin pathway.Journal of biomedical science · 2022Article
- Article
- Exosomal microRNA-588 from M2 polarized macrophages contributes to cisplatin resistance of gastric cancer cells.World journal of gastroenterology · 2021Article
- Ubiquitination and Deubiquitination in Oral Disease.International journal of molecular sciences · 2021Review
- Deubiquitinases: Modulators of Different Types of Regulated Cell Death.International journal of molecular sciences · 2021Review
- Stabilization of p18 by deubiquitylase CYLD is pivotal for cell cycle progression and viral replication.NPJ precision oncology · 2021Article
- CYLD Alterations in the Tumorigenesis and Progression of Human Papillomavirus-Associated Head and Neck Cancers.Molecular cancer research : MCR · 2021Review
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12 authors.
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Abstract
Cisplatin is one of the most effective chemotherapeutic agents commonly used for several malignancies including oral squamous cell carcinoma (OSCC). Although cisplatin resistance is a major obstacle to effective treatment and is associated with poor prognosis of OSCC patients, the molecular mechanisms by which it develops are largely unknown. Cylindromatosis (CYLD), a deubiquitinating enzyme, acts as a tumor suppressor in several malignancies. Our previous studies have shown that loss of CYLD expression in OSCC tissues is significantly associated with poor prognosis of OSCC patients. Here, we focused on CYLD expression in OSCC cells and determined whether loss of CYLD expression is involved in cisplatin resistance in OSCC and elucidated its molecular mechanism. In this study, to assess the effect of CYLD down-regulation on cisplatin resistance in human OSCC cell lines (SAS), we knocked-down the CYLD expression by using CYLD-specific siRNA. In cisplatin treatment, cell survival rates in CYLD knockdown SAS cells were significantly increased, indicating that CYLD down-regulation caused cisplatin resistance to SAS cells. Our results suggested that cisplatin resistance caused by CYLD down-regulation was associated with the mechanism through which both the reduction of intracellular cisplatin accumulation and the suppression of cisplatin-induced apoptosis via the NF-κB hyperactivation. Moreover, the combination of cisplatin and bortezomib treatment exhibited significant anti-tumor effects on cisplatin resistance caused by CYLD down-regulation in SAS cells. These findings suggest the possibility that loss of CYLD expression may cause cisplatin resistance in OSCC patients through NF-κB hyperactivation and may be associated with poor prognosis in OSCC patients.
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