Li Meng, Fan Yibin, Wang Yutong, Xu Jinhua, Xu Hui
Department of Dermatology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University, School of Medicine, Shanghai 200011, P.R. China.
Department of Dermatology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang 310014, P.R. China.
Exp Ther Med. 2020 Aug;20(2):1371-1378. doi: 10.3892/etm.2020.8849. Epub 2020 Jun 5.
Genome wide association studies have revealed that the zinc finger MIZ-type containing 1 (ZMIZ1) is involved in the pathogenesis of vitiligo; however, the underlying mechanism remains unclear. The present study aimed to investigate the effects of ZMIZ1 on the proliferation, apoptosis and migration of the human melanocyte cell lines PIG1 and PIG3V. ZMIZ1 overexpression and knockdown PIG1 and PIG3V cell models were established by lentivirus infection, and the effects of ZMIZ1 on cell proliferation and apoptosis were determined using an MTT assay and flow cytometry, respectively. Furthermore, the expression levels of proliferation- and apoptosis-associated proteins were analyzed using western blotting. Additionally, Transwell assays were performed to determine the effect of ZMIZ1 on the migration of PIG1 and PIG3V cells. Finally, the effect of ZMIZ1 on cytoskeletal remodeling in PIG1 and PIG3V cells was analyzed using immunocytochemistry. The overexpression of ZMIZ1 promoted the proliferation and inhibited the apoptosis of PIG1 and PIG3V cells, whereas the genetic knockdown of ZMIZ1 resulted in the opposite effects. Furthermore, ZMIZ1 overexpression increased the migration, whereas the knockdown of ZMIZ1 inhibited the migration and altered remodeling of the actin cytoskeleton in PIG1 and PIG3V cells. In conclusion, the results of the present study suggest that ZMIZ1 regulates the proliferation, apoptosis and migration of PIG1 and PIG3V cells, and indicate that ZMIZ1 may serve as a potential therapeutic target for vitiligo.
全基因组关联研究表明，含锌指MIZ型蛋白1（ZMIZ1）参与了白癜风的发病机制；然而，其潜在机制仍不清楚。本研究旨在探讨ZMIZ1对人黑素细胞系PIG1和PIG3V增殖、凋亡及迁移的影响。通过慢病毒感染建立ZMIZ1过表达和敲低的PIG1和PIG3V细胞模型，分别采用MTT法和流式细胞术检测ZMIZ1对细胞增殖和凋亡的影响。此外，用蛋白质印迹法分析增殖和凋亡相关蛋白的表达水平。另外，进行Transwell实验以确定ZMIZ1对PIG1和PIG3V细胞迁移的影响。最后，用免疫细胞化学法分析ZMIZ1对PIG1和PIG3V细胞细胞骨架重塑的影响。ZMIZ1的过表达促进了PIG1和PIG3V细胞的增殖并抑制了其凋亡，而ZMIZ1的基因敲低则产生相反的效果。此外，ZMIZ1的过表达增加了细胞迁移，而ZMIZ1的敲低则抑制了PIG1和PIG3V细胞的迁移并改变了肌动蛋白细胞骨架的重塑。总之，本研究结果表明ZMIZ1调节PIG1和PIG3V细胞的增殖、凋亡和迁移，并表明ZMIZ1可能作为白癜风的潜在治疗靶点。
