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.  https://www.selleckchem.com/products/Nolvadex.html  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.The high metastatic rate of breast cancer is the significant cause of its poor prognosis. The long noncoding RNA (lncRNA) proliferating cell nuclear antigen pseudogene 1 (PCNAP1) plays important roles in the initiation and progression of cancers; however, its regulatory function and molecular mechanism in breast cancer metastasis remains unknown. Therefore, we investigated the roles of lncRNA PCNAP1 in breast cancer metastasis by modulating the microRNA (miR)‑340‑5p/SOX4 axis using quantitative real‑time PCR, in vivo mouse models, nucleo‑cytoplasmic separation, western blot analysis, scratch assays, Transwell assays, luciferase reporter assays and MS2‑RIP, in vitro and in vivo. lncRNA PCNAP1 was found to be upregulated in human breast cancer tissues, and high lncRNA PCNAP1 levels predicted poor overall survival. Function assays showed that knockdown of lncRNA PCNAP1 suppressed the migration and invasion of breast cancer cells in vitro and in vivo. Mechanistically, lncRNA PCNAP1 functioned as a competing endogenous (ce)RNA for miR‑340‑5p to facilitate the expression of its target gene SRY‑box transcription factor 4 (SOX4), promoting migration and invasion of breast cancer cells. Overall, we found that lncRNA PCNAP1 predicted a poor prognosis in breast cancer and promoted cancer metastasis via miR‑340‑5p‑dependent upregulation of SOX4 expression. These results suggest that lncRNA PCNAP1 has potential as an alternative therapeutic target to suppress breast cancer metastasis.There have been few studies investigating the potential effects of indoor sources of particulate matter on human health. In this study, the effect of different concentrations of fine particulate matter (PM2.5) collected from a printing room on lung health was examined using cultured cells and a mouse model. Further, the mechanism of lung injury was examined. The results indicated that PM2.5 significantly enhanced malondialdehyde activity (P less then 0.05), decreased superoxide dismutase activity (P less then 0.05), upregulated the expression of pro‑inflammatory factors including interleukin (IL)‑1β, tumor necrosis factor‑, IL‑6 and downregulated the expression of the inflammatory factor IL‑2 (P less then 0.05). Western blot analysis indicated that PM2.5 significantly enhanced expression of phosphorylated (p)‑ERK relative to total ERK, cyclooxygenase‑2, p‑anti‑nuclear‑factor‑κB (p‑NF‑κB) relative to NF‑κB, transforming growth factor‑β1 and Bax relative to Bcl‑2 in inflammation (P less then 0.05), fibrosis and apoptosis signaling pathways. Furthermore, the results revealed that exposure was associated with an increased abundance of pathogens including Burkholderiales, Coriobacteriia, and Betaproteobacteria in in the lungs. In conclusion, exposure to PM2.5 from a printing room significantly increased inflammation, fibrosis, apoptosis and the abundance of pathogenic bacteria, indicating that exposure is potential threat to individuals who spend a significant amount of time in printing rooms.Gastric cancer (GC) is one of the most common causes of cancer‑related mortality worldwide. Despite remarkable progress in the diagnosis and treatment of GC, a large number of cases are diagnosed as advanced GC, and treatment failure occurs. Emerging evidence has shown that non‑coding RNAs (ncRNAs), especially microRNAs (miRNAs) and long non‑coding RNAs (lncRNAs), play a vital role in the tumorigenesis and development of GC. Moreover, the pathogenesis of GC is closely related to aberrant activation of the Wnt (Wingless‑type MMTV integration site family) signaling pathway. ncRNAs serve as potential novel biomarkers in the clinical examination, prognosis and therapeutic targeting of GC. Furthermore, dysregulation of ncRNAs has been demonstrated to affect tumor initiation, epithelial‑mesenchymal transition (EMT), angiogenesis, tumor development, invasion, metastasis and resistance to therapy via the Wnt/β‑catenin signaling pathway. This review focuses on the role of ncRNAs in modulating the Wnt/β‑catenin signaling pathway in the pathogenesis of GC, which may provide a reference for the clinical diagnosis and treatment of GC.Long non‑coding RNA (lncRNA) NR2F1 antisense RNA 1 (NR2F1‑AS1) has been reported to be an oncogene in several cancer types, including osteosarcoma (OS). However, the underlying fundamental molecular mechanism of NR2F1‑AS1 in OS remains largely unknown, which the present study aimed to elucidate. The present study demonstrated that NR2F1‑AS1 expression is markedly increased in OS, and NR2F1‑AS1 was shown to exert oncogenic functions in OS. Further molecular mechanistic studies revealed that microRNA (miR)‑485‑5p and miR‑218‑5p were direct targets of NR2F1‑AS1. More importantly, miR‑485‑5p and miR‑218‑5p exhibited low expression levels and were negatively correlated with NR2F1‑AS1 expression in OS tissues. It was then identified that baculoviral inhibitor of apoptosis repeat‑containing 5 (BIRC5) was a direct target of miR‑485‑5p and miR‑218‑5p in OS cells. Furthermore, a series of experiments suggested that NR2F1‑AS1 affects the proliferation, migration, invasion and apoptosis of OS cells by regulating BIRC5. Finally, it was revealed that silencing of NR2F1‑AS1 repressed the OS cell malignant phenotype by binding with miR‑485‑5p and miR‑218‑5p, and then downregulating BIRC5 expression, which suggests that the NR2F1‑AS1/miR‑485‑5p/miR‑218‑5p/BIRC5 axis could be a potential target for treating OS.