Interleukin-33 enhanced the migration and invasiveness of human lung cancer cells
Received 2 November 2017
Accepted for publication 15 December 2017
Published 16 February 2018 Volume 2018:11 Pages 843—849
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Justinn Cochran
Peer reviewer comments 2
Editor who approved publication: Dr Yao Dai
Zhiping Yang,1 Xin Gao,2 Jingyu Wang,3 Longsheng Xu,4 Ying Zheng,4 Yufen Xu1
1Department of Oncology (04-F-14), The First Affiliated Hospital of Jiaxing University, Jiaxing, 2Department of Oncology, Suzhou Municipal Hospital of Nanjing Medical University, Suzhou, 3Department of Pathology, 4Department of Central Laboratory, The First Affiliated Hospital of Jiaxing University, Jiaxing, People’s Republic of China
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 metalloproteinase (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.
Keywords: ST2, AKT, migration, invasion
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