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The functions of DEMs were evaluated using the tool for annotations of human miRNAs database, and via Gene Ontology analysis, Kyoto Encyclopedia of Genes and Genomes analysis and Gene Set Enrichment Analysis of the target genes. Finally, survival analyses of DEMs, which were in the miRNA-gene network, was performed. The results suggested that a number of miRNAs, including hsa-let-7a-5p, hsa-miR-27a-3p, hsa-miR-126-5p and hsa-miR-424-5p, may serve critical roles in EGC. The present study could provide a basis for the identification of EGC screening biomarkers. Furthermore, the present study may provide a basis for the exploration of the cause of the high incidence of gastric cancer in Gansu province from the perspective of miRNAs.Although targeted therapy has emerged as an effective treatment strategy for non-small cell lung cancer (NSCLC), some patients cannot benefit from such therapy due to the limited number of therapeutic targets. The present study aimed to identify mutated genes associated with clinicopathological characteristics and prognosis and to screen for mutations that are not concurrent with applicable drug target sites in patients with NSCLC. Tumor tissue and blood samples were obtained from 97 patients with NSCLC. A lung cancer-specific panel of 55 genes was established and analyzed using next-generation sequencing (NGS). The results obtained from the clinical cohort were compared with the NSCLC dataset from The Cancer Genome Atlas (TCGA). Subsequently, 25 driver genes were identified by taking the intersection of the 55 lung-cancer-specific genes with three databases, namely, the Catalog of Somatic Mutations in Cancer database, the Network of Cancer Genes database and Vogelstein’s list. Functional annotation and proteThus, the present study highlights the importance of NOTCH2 mutations and might provide novel therapeutic options for patients with NSCLC who do not harbor EGFR mutations.Long non-coding RNAs (lncRNAs) have attracted widespread attention as potential biological and pathological regulators. lncRNAs are involved in several biological processes in cancer. Triple negative breast cancer (TNBC) is characterized by strong heterogeneity and aggressiveness. At present, the implication of microRNAs (miRs) and lncRNAs in immunotherapy has been poorly studied. Nevertheless, the blockade of immune checkpoints, particularly that of the programmed cell-death protein-1/programmed cell-death ligand-1 (PD-L1) axis, is considered as a principle approach in breast cancer (BC) therapy. The present study aimed to investigate the interaction between immune-modulatory upstream signaling pathways of the PD-L1 transcript that could enhance personalized targeted therapy. MDA-MB-231 cells were transfected with miR-182-5p mimics followed by RNA extraction and cDNA synthesis using a reverse transcription kit, and the expression levels of the target genes were assessed by reverse transcription-quantitative PCR. Furthermore, the expression levels of target genes were measured in tissues derived from 41 patients with BC, including patients with luminal BC and TNBC, as well as their adjacent lymph nodes. The results revealed that the expression levels of miR-182-5p, PD-L1 and metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) were upregulated in MDA-MB-231 cells and BC tissues. However, X-inactive specific transcript (XIST) expression was downregulated in cancer tissues and TNBC cells. Following co-transfection of cells with small interfering RNAs specific for each target gene and miR-182-5p antagomirs, the effect of miR-182-5p was abolished in the presence of lncRNAs. Therefore, the results of the present study indicated that although miR-182-5p exhibited an oncogenic effect, XIST exerted a dominant effect on the regulation of the PD-L1 signaling pathway via the inhibition of the oncogenic function of MALAT1.[This corrects the article DOI 10.3892/ol.2017.6106.].MicroRNAs (miRNAs) are involved in the development of non-small cell lung cancer (NSCLC). However, the biological roles of several aberrantly expressed miRNAs have not been explored yet. In the present study, miR-4491 was identified as a novel upregulated miRNA in NSCLC tissues and cell lines. Downregulation of miR-4491 by a miR-4491 inhibitor inhibited the proliferation and triggered the apoptosis of NSCLC cells. Tripartite motif containing 7 (TRIM7), a tumor suppressor gene expressed in NSCLC, was demonstrated in the present study to be directly targeted by miR-4491. This finding was verified by bioinformatics analysis, reverse transcription-quantitative PCR, western blotting and dual luciferase reporter assays. Furthermore, downregulation of miR-4491 inactivated nuclear factor-κB signaling via induction of TRIM7. In addition, TRIM7 silencing attenuated the effect of miR-4491 inhibitor in NSCLC cells. The decreased TRIM7 level in NSCLC tissues was negatively correlated with miR-4491 expression in NSCLC tissues. selleck chemicals llc In conclusion, the findings from this study demonstrated that miR-4491 expression was upregulated in NSCLC tissues and cells and that miR-4491 may promote NSCLC progression via targeting TRIM7.Differentiated thyroid cancer (DTC) is the most frequent endocrine tumor with a good prognosis after primary treatment in most cases. By contrast, 30-40% of patients with metastatic DTC are unresponsive to 131I radioactive iodide (RAI) treatment due to tumor dedifferentiation. Currently, underlying molecular mechanisms of dedifferentiation remain elusive and predictive biomarkers are lacking. Therefore, the present study aimed to identify molecular biomarkers in primary tumors associated with RAI refractoriness. A retrospective cohort was gathered consisting of RAI-sensitive patients with DTC and RAI-refractory patients with poorly DTC. In all patients, extensive intratumoral mutation profiling, gene fusions analysis, telomerase reverse transcriptase (TERT) promoter mutation analysis and formalin-fixed paraffin-embedded-compatible RNA sequencing were performed. Genetic analyses revealed an increased mutational load in RAI-refractory DTC, including mutations in AKT1, PTEN, TP53 and TERT promoter. Transcriptomic analyses revealed profound differential expression of insulin-like growth factor 2 (IGF2), with up to 100-fold higher expression in RAI-refractory DTC compared with in RAI-sensitive DTC cases.