ZMIZ1 promotes the proliferation and migration of melanocytes in vitiligo
- Meng Li
- Yibin Fan
- Yutong Wang
- Jinhua Xu
- Hui Xu
Affiliations: 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, Department of Dermatology, Huashan Hospital, Fudan University, Shanghai 200041, P.R. China
- Published online on: June 5, 2020 https://doi.org/10.3892/etm.2020.8849
Copyright: © Li
et al. This is an open access article distributed under the
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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.