ArticleOncotarget2016
Interleukin-32α induces migration of human melanoma cells through downregulation of E-cadherin.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Interleukin 32 Exacerbates Vitiligo by Promoting Inflammation and Oxidative Stress-induced Injury in Melanocytes.Inflammation · 2026Article
- IL-32 as a potential biomarker and therapeutic target in skin inflammation.Frontiers in immunology · 2023Review
- Identification of molecular subtyping system and four-gene prognostic signature with immune-related genes for uveal melanoma.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Interleukin-32 regulates downstream molecules and promotes the invasion of pancreatic cancer cells.Oncology letters · 2022Article
- Melanoma Progression under Obesity: Focus on Adipokines.Cancers · 2021Review
- Cell Adhesion Molecules in Plasticity and Metastasis.Molecular cancer research : MCR · 2021Review
- Article
- Interleukin 32 expression in human melanoma.Journal of translational medicine · 2019Article
- Inhibition of skin carcinogenesis by suppression of NF-κB dependent ITGAV and TIMP-1 expression in IL-32γ overexpressed condition.Journal of experimental & clinical cancer research : CR · 2018Article
- Role of interleukin-32 in cancer biology.Oncology letters · 2018Review
- Elevated Gene Expression of Interleukin-32 Isoforms Alpha, Beta, Gamma, and Delta in the Peripheral Blood of Chronic Psoriatic Patients.Diseases (Basel, Switzerland) · 2018Article
- Article
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin (IL)-32α, the shortest isoform of proinflammatory cytokine IL-32, is associated with various inflammatory diseases and cancers. However, its involvement in human melanoma is not understood. To determine the effect of IL-32α in melanoma, IL-32α levels were examined in human melanoma cell lines that exhibit different migratory abilities. IL-32α levels were higher in human melanoma cell lines with more migratory ability. An IL-32α-overexpressing G361 human melanoma cell line was generated to investigate the effect of IL-32α on melanoma migration. IL-32α-overexpressing G361 cells (G361-IL-32α) exhibit an increased migratory ability compared to vector control cells (G361-vector). To identify factors involved in IL-32α-induced migration, we compared expression of E-cadherin in G361-vector and G361-IL-32α cells. We observed decreased levels of E-cadherin in G361-IL-32α cells, resulting in F-actin polymerization. To further investigate signaling pathways related to IL-32α-induced migration, we treated G361-vector and G361-IL-32α cells with PD98059, a selective MEK inhibitor. Inhibition of Erk1/2 by PD98059 restored E-cadherin expression and decreased IL-32α-induced migration. In addition, cell invasiveness of G361-IL-32α cells was tested using an in vivo lung metastasis model. As results, lung metastasis was significantly increased by IL-32α overexpression. Taken together, these data indicate that IL-32α induced human melanoma migration via Erk1/2 activation, which repressed E-cadherin expression. Our findings suggest that IL-32α is a novel regulator of migration in melanoma.
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