Knockdown of USP8 Inhibits the Growth of Lung Cancer Cells

Zhenhua Rong,1 Zongmin Zhu,2 Shihua Cai,3 Bingqing Zhang4 1Minimally Invasive Surgery Oncology, The People’s Hospital of Caoxian, Heze, Shandong, People’s Republic of China; 2Department of Pharmacology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250011, People’s Republic of China; 3Department of Outpatient, Heze Municipal Hospital, Heze 274000, Shandong, People’s Republic of China; 4Department of Respiratory Medicine, Heze Municipal Hospital, Heze 274000, Shandong, People’s Republic of ChinaCorrespondence: Bingqing ZhangDepartment of Respiratory Medicine, Heze Municipal Hospital, No. 2888 Caozhou Road, Peony District, Heze 274000, Shandong, People’s Republic of ChinaEmail hzzhangbq@163.comPurpose: Lung cancer is the deadliest tumor in the world. This study aimed to investigate the effection of USP8 on the proliferation and growth of NSCLC cells.Methods: The proliferation, migration, invasion, cell cycle progression, and apoptosis of A549 and H1299 cells were evaluated with CCK8, colony formation, scratch, transwell, and flow cytometry experiments. Furthermore, the expression of cell cycle- and apoptosis-related proteins was detected by western blot.Results: Knockdown of USP8 inhibited the proliferation, migration, invasion, and cell cycle progression of A549 and H1299 cells, and promoted the apoptosis. The results of western blot indicated that knockdown of USP8 down-regulated the expression of Cyclin D1, CDK4, CDK6, p-AKT, and Bcl2, and up-regulated the expression of Bax.Conclusion: Knockdown of USP8 inhibited the proliferation of human lung cancer cells by regulating cell cycle- and apoptosis-related proteins. USP8 may be a therapeutic target for lung cancer.Keywords: apoptosis, lung cancer, PI3K/AKT pathway, proliferation, USP8