ArticleOncogene2016
CD82 suppresses CD44 alternative splicing-dependent melanoma metastasis by mediating U2AF2 ubiquitination and degradation.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 43 citations in OpenAlex.
- U2AF2-regulated alternative splicing of UPP1 promotes NSCLC progression by enhancing glycolysis.Cell communication and signaling : CCS · 2026Article
- mCellular & molecular biology letters · 2026Article
- THOC1 binds to U2AF2 and regulates ovarian cancer progression through the beta-catenin / c-myc / cyclinD1 signaling pathway.Cancer cell international · 2025Article
- HPGD induces ferroptosis and autophagy to suppress esophageal squamous cell carcinoma through the LXA4-ERK1/2-U2AF2-TFRC axis.Molecular cancer · 2025Article
- Splicing regulatory dynamics for precision analysis and treatment of heterogeneous leukemias.Science translational medicine · 2025Article
- Comprehensive systems biology analysis reveals splicing factor contributions to cutaneous melanoma progression.Scientific reports · 2025Article
- CD82-associated exhausted CD8Frontiers in immunology · 2025Article
- U2AF2-SNORA68 promotes triple-negative breast cancer stemness through the translocation of RPL23 from nucleoplasm to nucleolus and c-Myc expression.Breast cancer research : BCR · 2024Article
- Roles and mechanisms of aberrant alternative splicing in melanoma - implications for targeted therapy and immunotherapy resistance.Cancer cell international · 2024Review
- New Functions of Intracellular LOXL2: Modulation of RNA-Binding Proteins.Molecules (Basel, Switzerland) · 2023Article
- Identification of Alternative Splicing in Proteomes of Human Melanoma Cell Lines without RNA Sequencing Data.International journal of molecular sciences · 2023Article
- Multi-omics analysis of the Indian ovarian cancer cohort revealed histotype-specific mutation and gene expression patterns.Frontiers in genetics · 2023Article
- RNA-binding proteins regulating the CD44 alternative splicing.Frontiers in molecular biosciences · 2023Review
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- Review
- Review
- TGF-β1 promotes epithelial-to-mesenchymal transition and stemness of prostate cancer cells by inducing PCBP1 degradation and alternative splicing of CD44.Cellular and molecular life sciences : CMLS · 2021Article
- Dual Antimicrobial and Antiproliferative Activity of TcPaSK Peptide Derived from aMicroorganisms · 2021Article
- Role of Metastasis Suppressor KAI1/CD82 in Different Cancers.Journal of oncology · 2021Review
- The U2AF2 /circRNA ARF1/miR-342-3p/ISL2 feedback loop regulates angiogenesis in glioma stem cells.Journal of experimental & clinical cancer research : CR · 2020Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Melanoma is one of the most lethal forms of skin cancer because of its early metastatic spread. The variant form of CD44 (CD44v), a cell surface glycoprotein, is highly expressed on metastatic melanoma. The mechanisms of regulation of CD44 alternative splicing in melanoma and its pathogenic contributions are so far poorly understood. Here, we investigated the expression level of CD44 in a large set of melanocytic lesions at different stages. We found that the expression of CD44v8-10 and a splicing factor, U2AF2, is significantly increased during melanoma progression, whereas CD82/KAI1, a tetraspanin family of tumor suppressor, is reduced in metastatic melanoma. CD44v8-10 and U2AF2 expression levels, which are negatively correlated with CD82 levels, are markedly elevated in primary melanoma compared with dysplastic nevi and further increased in metastatic melanoma. We also showed that patients with higher CD44v8-10 and U2AF2 expression levels tended to have shorter survival. By using both in vivo and in vitro assays, we demonstrated that CD82 inhibits the production of CD44v8-10 on melanoma. Mechanistically, U2AF2 is a downstream target of CD82 and in malignant melanoma facilitates CD44v8-10 alternative splicing. U2AF2-mediated CD44 isoform switch is required for melanoma migration in vitro and lung and liver metastasis in vivo. Notably, overexpression of CD82 suppresses U2AF2 activity by inducing U2AF2 ubiquitination. In addition, our data suggested that enhancement of melanoma migration by U2AF2-dependent CD44v8-10 splicing is mediated by Src/focal adhesion kinase/RhoA activation and formation of stress fibers, as well as CD44-E-selectin binding reinforcement. These findings uncovered a hitherto unappreciated function of CD82 in severing the linkage between U2AF2-mediated CD44 alternative splicing and cancer aggressiveness, with potential prognostic and therapeutic implications in melanoma.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.