Background Melanoma is one of the most lethal tumors and its treatment is still challenging. It is urgent to detect novel therapy targets in melanoma. Material/Methods The GEO dataset was used to obtain a list of DEGS (differentially-expressed genes). Integrative bioinformatics analyses, including HPRD database, TCGA data, and TIMER, were performed to determine the role of CXCL13 in SKCM (skin cutaneous melanoma) progression and the immune environment. Furthermore, Pearson correlation coefficient analysis was used to measure correlations between CXCL13 and its co-expressed genes. Survival analysis, GO, and KEGG enrichment analysis were performed to investigate the role of CXCL13 in SKCM. Results A total of 41 DEGs were identified in 3 GEO datasets, and 4 out of 41 DEGs are hub genes. Among the 4 hub genes, CXCL13 is involved in the most KEGG terms. CXCL13 is co-expressed with well-known immune checkpoint blockade targets, and it was associated with better overall survival. In addition, CXCL13 levels in infiltrating immune cells (neutrophil and myeloid dendritic cells) affect prognosis and survival in SKCM. Functional enrichment analysis clarified that CXCL13- co-expressed top 30 genes were associated with immune signaling pathways. Network analysis identified CXCL13 as a hub gene that interacts with CXCR5 to participate in immune-related biological process. Conclusions This study found that CXCL13 is associated with SKCM tumorigenesis and prognosis and immune infiltrations. Our result suggests that CXCL13 has great potential in development of novel immunotherapy targets in melanoma.

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Osteosarcoma (OS) is a severe disease that is generally caused by genetic alterations. Systematic identification of driver genes may be used to increase the understanding of the mechanisms underlying the disease. The present study identified a framework to predict driver genes, with the hypothesis that driver genes operate through a number of connected functional genes. OS-related genes were extracted from the Catalogue Of Somatic Mutations In Cancer and subsequently ranked by virtue of their effect on a set of functional genes using a network-based algorithm. This revealed the driver genes associated with dysregulated networks. In addition, compared with the Mutations For Functional Impact on Network Neighbors algorithm, the results obtained using the aforementioned network-based algorithm revealed that the proposed method is effective. Gene functional analysis demonstrated that the potential OS driver genes were involved in OS-associated pathways. Through the validation of the 15 candidate OS driver genes, the classifier constructed in the present study revealed that the identified driver genes were able to distinguish 184 cancer samples from controls. Therefore, the present study provided insights into the identification of driver genes from a vast amount of sequencing data.