IFN-γ induces apoptosis in human melanocytes by activating the JAK1/STAT1 signaling pathway

The present study aimed to investigate the role of janus kinase (JAK)1/STAT1 in interferon (IFN)-γ-induced apoptosis in human melanocytes. Following IFN-γ treatment, the viability of human melanocytes were analyzed using a Cell Counting Kit-8 assay and the apoptotic rate was determined using flow cytometry. Western blotting was also performed to analyze the phosphorylation levels of JAK1, JAK2 and the transcriptional factor STAT1, as well as the expression levels of Bcl-2, Bax, Bcl-2 homologous antagonist killer (Bak) and cleaved caspase-3. Finally, following the pretreatment with the STAT1 inhibitor fludarabine, human melanocytes were treated with IFN-γ and flow cytometry was used to detect the apoptotic rate. The results revealed that IFN-γ reduced the proliferation and induced the apoptosis of human melanocytes. In addition, IFN-γ treatment led to decreased expression levels of Bcl-2 and increased expression levels of Bax, Bak and cleaved caspase-3, alongside the activation of the JAK1/STAT1 signaling pathway. Conversely, the pretreatment with the STAT1 inhibitor fludarabine decreased the apoptotic rate of human melanocytes following IFN-γ induction. In conclusion, the findings of the present study suggested that IFN-γ may induce the apoptosis of human melanocytes by activating the JAK1/STAT1 signaling pathway, alongside increasing the expression levels of Bax, Bak and cleaved caspase-3, and decreasing the expression levels of Bcl-2.