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Interleukin-33 enhanced the migration and invasiveness of human lung cancer cells

AIM: Interleukin-33 (IL-33), belonging to IL-1 family cytokines, has been reported to participate in cancer growth and metastasis. The clinical values of IL-33 in lung cancer have been previously investigated. We aimed to elucidate the probable role of IL-33 in the migration and invasion of lung can...

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Detalles Bibliográficos
Autores principales: Yang, Zhiping, Gao, Xin, Wang, Jingyu, Xu, Longsheng, Zheng, Ying, Xu, Yufen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5820469/
https://www.ncbi.nlm.nih.gov/pubmed/29497316
http://dx.doi.org/10.2147/OTT.S155905
Descripción
Sumario:AIM: Interleukin-33 (IL-33), belonging to IL-1 family cytokines, has been reported to participate in cancer growth and metastasis. The clinical values of IL-33 in lung cancer have been previously investigated. We aimed to elucidate the probable role of IL-33 in the migration and invasion of lung cancer cells. METHODS: Cell migration and invasiveness were tested by Transwell assay. Western blotting analysis was performed to detect protein expression. RESULTS: We found that IL-33 treatment in human lung A549 cells dose-dependently enhanced their migratory and invasive ability, accompanied by elevated expression of matrix metallo-proteinase (MMP) 2 and MMP9. Meanwhile, IL-33-induced cell migration and invasion were significantly abolished by small interfering RNA-targeting ST2, the specific receptor of IL-33. Furthermore, IL-33 exposure induced the phosphorylation of AKT. Pretreatment with an AKT inhibitor LY294002 markedly attenuated IL-33-induced cell migration and invasion. CONCLUSION: IL-33/ST2 promoted the migration and invasiveness of lung cancer cells through AKT pathway. Our findings strongly suggest that IL-33 may serve as a promising therapeutic strategy for lung cancer.