Rong Zhenhua, Zhu Zongmin, Cai Shihua, Zhang Bingqing
Minimally Invasive Surgery Oncology, The People's Hospital of Caoxian, Heze, Shandong, People's Republic of China.
Department of Pharmacology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250011, People's Republic of China.
Cancer Manag Res. 2020 Dec 2;12:12415-12422. doi: 10.2147/IJN.S259191. eCollection 2020.
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.
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.
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.
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.
肺癌是全球最致命的肿瘤。本研究旨在探讨泛素特异性蛋白酶8（USP8）对非小细胞肺癌（NSCLC）细胞增殖和生长的影响。
通过CCK8、集落形成、划痕、Transwell和流式细胞术实验评估A549和H1299细胞的增殖、迁移、侵袭、细胞周期进程和凋亡。此外，通过蛋白质免疫印迹法检测细胞周期和凋亡相关蛋白的表达。
敲低USP8可抑制A549和H1299细胞的增殖、迁移、侵袭及细胞周期进程，并促进细胞凋亡。蛋白质免疫印迹结果表明，敲低USP8可下调细胞周期蛋白D1（Cyclin D1）、细胞周期蛋白依赖性激酶4（CDK4）、细胞周期蛋白依赖性激酶6（CDK6）、磷酸化蛋白激酶B（p-AKT）和B细胞淋巴瘤/白血病-2（Bcl2）的表达，并上调Bax的表达。
敲低USP8通过调节细胞周期和凋亡相关蛋白抑制人肺癌细胞的增殖。USP8可能是肺癌的一个治疗靶点。
