ArticleThe Journal of investigative dermatology2013
CYLD inhibits melanoma growth and progression through suppression of the JNK/AP-1 and β1-integrin signaling pathways.
Article in The Journal of investigative dermatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed.
- OTUD4 stabilizes CYLD and counteracts BCL3 K63-linked polyubiquitination to suppress melanoma progression.Cell death & disease · 2026Article
- Targeting programmed cell death: a novel therapeutic paradigm for cancer based on mode-of-death classification.Apoptosis : an international journal on programmed cell death · 2026Review
- Role of LIGHT in the Inflammatory Mechanisms of Psoriasis via Upregulation of Proliferation and Cytokine Production of Keratinocytes.Immunity, inflammation and disease · 2026Article
- The role of non-coding RNAs in the regulation of cell death pathways in melanoma.Discover oncology · 2025Review
- Article
- Emerging roles of deubiquitinating enzymes in actin cytoskeleton and tumor metastasis.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- Melanoma biology and treatment: a review of novel regulated cell death-based approaches.Cancer cell international · 2024Review
- Southern rice black-streaked dwarf virus induces incomplete autophagy for persistence in gut epithelial cells of its vector insect.PLoS pathogens · 2023Article
- Necroptosis: A Pathogenic Negotiator in Human Diseases.International journal of molecular sciences · 2022Review
- Review
- Impact ofInternational journal of molecular medicine · 2022Article
- Analysis and identification of the necroptosis landscape on therapy and prognosis in bladder cancer.Frontiers in genetics · 2022Article
- Integrated analysis of necroptosis-related genes for evaluating immune infiltration and colon cancer prognosis.Frontiers in immunology · 2022Article
- Integrated Analysis of Necroptosis-Related Genes for Prognosis, Immune Microenvironment Infiltration, and Drug Sensitivity in Colon Cancer.Frontiers in medicine · 2022Article
- Development and Validation of a Novel Survival Model for Cutaneous Melanoma Based on Necroptosis-Related Genes.Frontiers in oncology · 2022Article
- Application of Regulatory Cell Death in Cancer: Based on Targeted Therapy and Immunotherapy.Frontiers in immunology · 2022Review
- Identification and Quantification of Necroptosis Landscape on Therapy and Prognosis in Kidney Renal Clear Cell Carcinoma.Frontiers in genetics · 2022Article
- The potential role of necroptosis in clinical diseases (Review).International journal of molecular medicine · 2021Review
- CYLD mutation characterizes a subset of HPV-positive head and neck squamous cell carcinomas with distinctive genomics and frequent cylindroma-like histologic features.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021Article
- CYLD Alterations in the Tumorigenesis and Progression of Human Papillomavirus-Associated Head and Neck Cancers.Molecular cancer research : MCR · 2021Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
The molecular mechanisms mediating cylindromatosis (CYLD) tumor suppressor function appear to be manifold. Here, we demonstrate that, in contrast to the increased levels of phosphorylated c-Jun NH(2)-terminal kinase (pJNK), CYLD was decreased in a majority of the melanoma cell lines and tissues examined. Exogenous expression of CYLD but not its catalytically deficient mutant markedly inhibited melanoma cell proliferation and migration in vitro and subcutaneous tumor growth in vivo. In addition, the melanoma cells expressing exogenous CYLD were unable to form pulmonary tumor nodules following tail-vein injection. At the molecular level, CYLD decreased β1-integrin and inhibited pJNK induction by tumor necrosis factor-α or cell attachment to collagen IV. Moreover, CYLD induced an array of other molecular changes associated with modulation of the "malignant" phenotype, including a decreased expression of cyclin D1, N-cadherin, and nuclear Bcl3, and an increased expression of p53 and E-cadherin. Most interestingly, coexpression of the constitutively active MKK7 or c-Jun mutants with CYLD prevented the above molecular changes, and fully restored melanoma growth and metastatic potential in vivo. Our findings demonstrate that the JNK/activator protein 1 signaling pathway underlies the melanoma growth and metastasis that are associated with CYLD loss of function. Thus, restoration of CYLD and inhibition of JNK and β1-integrin function represent potential therapeutic strategies for treatment of malignant melanoma.
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