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Background Kang-bai-ling (KBL), a Chinese patent medicine, has been demonstrated as an effective therapy for vitiligo in China. However, the pharmacological mechanisms of KBL have not been completely elucidated. Methods In this study, the potential multicomponent, multitarget, and multipathway mechanism of KBL against vitiligo was clarified by using network pharmacology-based strategy. In brief, potential targets of KBL were collected based on TCMSP databases, followed by network establishment concerning the interactions of potential targets of KBL with well-known therapeutic targets of vitiligo by using protein-protein interaction (PPI) data. As a result, key nodes with higher level of seven topological parameters, including “degree centrality (DC),” “betweenness centrality (BC),” “closeness centrality (CC),” “eigenvector centrality (EC),” “network centrality (NC),” and “local average connectivity (LAC)” were identified as the main targets in the network, followed by subsequent incorporation into the ClueGO for GO and KEGG signaling pathway enrichment analysis. Results In accordance with the topological importance, a total of 23 potential targets of KBL on vitiligo were identified as main hubs. Additionally, enrichment analysis suggested that targets of KBL on vitiligo were mainly clustered into multiple biological processes (associated with DNA translation, lymphocyte differentiation and activation, steroid biosynthesis, autoimmune and systemic inflammatory reaction, neuron apoptosis, and vitamin deficiency) and related pathways (TNF, JAK-STAT, ILs, TLRs, prolactin, and NF-κB), indicating the underlying mechanisms of KBL on vitiligo. Conclusion In this work, we successfully illuminated the “multicompounds, multitargets” therapeutic action of KBL on vitiligo by using network pharmacology. Moreover, our present outcomes might shed light on the further clinical application of KBL on vitiligo treatment.

Background: Accumulating evidence announces that aberrantly expressed circRNAs were closely related to the development of human cancers. However, the role and mechanism of multiple circRNAs remain unclear. Our work aimed to disclose the functional role and mechanism of circ_0081054 in melanoma. Methods:Quantitative real-time polymerase chain reaction assay was utilized to detect circ_0081054, microRNA-637 (miR-637) and RAB9A (member RAS oncogene family) mRNA expression. Cell proliferative ability was evaluated via Cell Counting Kit-8 and colony formation assay. Cell invasion was assessed by using wound healing assay. Results:The significant upregulation of circ_0081054 was detected in melanoma tissues and cells. The proliferation, migration, glycolytic metabolism, and angiogenesis in melanoma cells were suppressed, while apoptosis was promoted following the silence of circ_0081054. In addition, circ_0081054 could target miR-637, and miR-637 inhibitor could reverse the effects of circ_0081054 deficiency. Furthermore, RAB9A was a target gene for miR-637 and RAB9A overexpression could reverse the effects of miR-637 overexpression. In addition, the deficiency of circ_0081054 hampered tumor growth in vivo. Moreover, circ_0081054 could regulate RAB9A expression by sponging miR-637. Conclusion:All results indicated that circ_0081054 promoted the malignant behaviors of melanoma cells partly by regulating the miR-637/RAB9A molecular axis.