IL-33 Promotes the Growth of Non-Small Cell Lung Cancer Cells Through Regulating miR-128-3p/CDIP1 Signalling Pathway
Authors Zhou X, Feng Y, Liu S, Li C, Teng Y, Li X, Lu J
Received 20 August 2020
Accepted for publication 7 January 2021
Published 12 March 2021 Volume 2021:13 Pages 2379—2388
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Seema Singh
Xiaorong Zhou, 1,* Yuxu Feng, 2,* Siwen Liu, 1 Chenchen Li, 1 Yue Teng, 1 Xiaoyou Li, 1 Jianwei Lu 1
1Department of Medical Oncology, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, 210009 Jiangsu Province, People’s Republic of China; 2Department of Orthopedics, The Pukou Centre Hospital, Nanjing, 210009 Jiangsu Province, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Xiaoyou Li; Jianwei Lu
Department of Medical Oncology, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, No. 42 Baiziting, Xuanwu District, Nanjing 210009, Jiangsu Province, People’s Republic of China
Email [email protected]; [email protected]
Background: Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer-related deaths, and it is also the most frequently diagnosed cancer. Previous studies indicate that IL-33 plays a crucial role in the development of NSCLC. In recent years, the role of miRNAs in cancer has become increasingly clear. However, reports focused on the relation between IL-33 and miRNAs in NSCLC have been limited.
Methods: The expression of IL-33 and miR-128-3p was detected by qPCR. MTT, EdU, and colony formation assays were used to detect the proliferation ability of NSCLC cells. Transwell assay was used to investigate the migration and invasion of NSCLC cells. The expression of bax, cyt-c, and caspase 3 was detected by Western blot. Finally, in vivo tumor xenograft was used to detect the effects of IL-33 and miR-128-3p on tumor growth capacity.
Results: IL-33 was notably increased in the serum and tumor tissue of NSCLC patients. The in vitro function study revealed that IL-33 significantly promotes the proliferation, migration, and invasion of the NSCLC cells. In vivo experiments further confirmed the pro-tumor effect of IL-33 on NSCLC. The study on the underlying mechanism elucidated that IL-33 regulates the expression of miR-128-3p, which can directly target and inhibit the expression of CDIP1. Furthermore, IL-33 regulates the expression of downstream apoptotic proteins such as bax, cyt-c, and caspase3. Rescue experiments demonstrated that miR-28-3p can reverse the effect of IL-33.
Conclusion: These findings indicated that IL-33 and miR-128-3p may play a potential role in the diagnosis and treatment of NSCLC.
Keywords: IL-33, NSCLC, miR-128-3p, CDIP1
Corrigendum for this paper has been published
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