Lung cancer has the highest incidence and mortality rates of all cancers in China. Immune-related genes and immune infiltrating lymphocytes are involved in tumor growth, and in the past decade, immunotherapy has become increasingly important in the treatment of lung cancer. Using the edgeR package, differentially expressed genes and immune-related genes (DEIRGs) were identified in patients with lung adenocarcinoma (LUAD). Functional enrichment analysis of DEIRGs was performed using Gene Ontology annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. Survival-associated immune-related genes (IRGs) were selected using univariate Cox regression analysis and the prognostic model was assessed using multivariate Cox regression analysis. Overall, 273 DEIRGs were identified in LUAD, and KEGG pathway analysis of IRGs showed that 'cytokine-cytokine receptor interaction' was the most significantly enriched pathway. Furthermore, six survival associated IRGs were screened to establish a prognostic model; patients in the high risk score group had less favorable survival times, and the prognostic model was negatively associated with B cell infiltration. The present study established a prognostic model using analysis of survival-related immune-related genes, which were associated with B cell infiltration.

Breast cancer is the most common malignancy in women and microRNA-768-3p (miR-768-3p) is abnormally expressed in hepatocellular carcinoma, non-small cell lung carcinomas and melanoma. The aim of the present study was to evaluate the prognostic value and biological function of miR-768-3p in breast cancer. The expression of miR-768-3p in tumor tissues and adjacent tissues of 116 patients with breast cancer obtained by surgery and normal breast cell lines MCF-10A and breast cancer cell lines (MCF-7, MDA-MB-231, T-47D and SK-BR-3) were detected by reverse transcription-quantitative PCR. The association between miR-768-3p expression and the clinicopathological characteristics of patients was analyzed using the χ2 test. In addition, the Kaplan-Meier method was used for survival analysis. A Cox regression model was used to examine the effect of miR-768-3p on the prognosis of patients with breast cancer. Hemocytometer cell counting and Transwell assays were used to detect the effects of miR-768-3p on the characteristics of breast cancer cells. The target genes of miR-768-3p in breast cancer were identified by bioinformatics software and detected by luciferase reporter assay. Compared with normal tissues and normal breast cancer cells, miR-768-3p was significantly decreased in breast cancer tissues and cancer cells (P<0.001). The reduction in miR-768-3p was significantly associated with lymph node metastasis (P=0.040), Tumor Node Metastasis stage (P=0.035), and cancer subtype (P=0.008). In addition, patients with low miR-768-3p expression had a shorter overall survival time (log-rank P=0.022) compared with those with high expression and miR-768-3p may be a potential prognostic marker (hazard ratio=4.637; 95% confidence interval=1.296-16.597; P=0.018). When transfected with miR-768-3p inhibitor, cell viability, migration and invasion were significantly promoted compared with the control group (P<0.05). In addition, eukaryotic translation initiation factor 4E (eIF4E) was the target gene of miR-768-3p in breast cancer. All experiments confirmed that miR-768-3p, a tumor suppressor, inhibited the viability, migration and invasion of breast cancer cells through eIF4E. miR-768-3p may be a potential prognostic marker of breast cancer and may participate in the progression of breast cancer.

Melanoma is the most lethal cutaneous cancer with a high metastatic rate worldwide, causing ~55,500 deaths annually. Although the selective B-Raf oncogene serine/threonine-kinase (BRAF) inhibitors, dabrafenib and vemurafenib, have been approved for the treatment of BRAF-mutant metastatic melanoma, the 5-year survival rate remains unfavorable due to acquired therapy resistance. Therefore, it is of great importance to develop alternative therapeutic drugs and uncover their mechanisms for the treatment of melanoma. 7-dehydrocholesterol (7-DHC) has been demonstrated to inhibit melanoma, but the mechanism is unclear. Therefore, the present study aimed to elucidate the mechanisms of the inhibitory effect of 7-DHC in melanoma cells via analyzing the proliferation, migration, apoptosis, cell cycle and transcriptional sequencing of melanoma cells treated with 7-DHC, as well as constructing a gene signature according to public data of patients with melanoma. In the present study, 7-DHC, the precursor of vitamin D3, was able to induce apoptosis and inhibit cell proliferation and invasion of melanoma cells in a dose-dependent manner. RNA sequencing of melanoma cells treated with different concentrations of 7-DHC revealed that, compared with untreated melanoma cells, 65 genes were downregulated, and genes involved in the regulation of NF-ĸB import into the nucleus and NF-ĸB signaling were significantly repressed. Consistently, the Akt kinase family was one of most common somatic mutation hotspots in patients with melanoma according to The Cancer Genome Atlas enrichment analysis. Furthermore, 7-DHC decreased the phosphorylation of Akt1-Ser473 rather than that of MEK1, and the decreased phosphorylation of Akt1 subsequently inhibited the translocation of free RELA proto-oncogene NF-κB subunit to the nucleus. Finally, by intersecting downregulated genes by 7-DHC treatment and upregulated genes in patients with melanoma, a 7-DHC gene signature was identified, which was negatively associated with the prognosis. Overall, the present results demonstrated that 7-DHC suppressed melanoma cell proliferation and invasion via the Akt1/NF-ĸB signaling pathway, and 7-DHC key target genes were negatively associated with the prognosis. These findings highlight the potential application of 7-DHC for the treatment of melanoma in the future.