BackgroundThe expression of miR-205 is closely related to the occurrence, development, and prognosis of lung cancer and breast cancer. However, studies show that it plays opposite roles in different tumor types. Because the expression and regulation of miR-205 are primarily confined to epigenetic areas, whether genetic variation of miR-205 is related to the occurrence or to the development of tumors has not been reported. The aim of this study was to screen genetic variation of miR-205 gene and to investigate its association with the risk and development of lung and breast cancer.Material/MethodsGenomic DNA was extracted from cultured tumor cell lines and formalin-fixed and paraffin-embedded lung and breast tissue samples. Bisulfite Clone Sequencing (BCS) and qRT-PCR were employed to detect the DNA methylation status and gene expression of the miR-205 gene, respectively. Genetic variation of miR-205 and miR-205HG were genotyped with PCR-sequencing method. Immunohistochemical analysis for ER, PR, and HER2 was performed on breast tissue samples.ResultsA polymorphism, rs3842530, located downstream of the miR-205 gene and in the fourth exon of the miR-205 host gene (miR-205HG), was screened. rs3842530 had no correlation with the risk of breast cancer, but was associated with the risk of lung cancer (P<0.05).ConclusionsThese results indicate that the functional association of rs3842530 in miR-205HG and lung cancer might provide a possible explanation for the tissue-dependent function of miR-205 in different tumors.

Purpose. We apply the bioinformatics method to excavate the potential genes and therapeutic targets associated with valvular atrial fibrillation (VAF). Methods. The downloaded gene expression files from the gene expression omnibus (GEO) included patients with primary severe mitral regurgitation complicated with sinus or atrial fibrillation rhythm. Subsequently, the differential gene expression in left and right atrium was analyzed by R software. Additionally, weighted correlation network analysis (WGCNA), principal component analysis (PCA), and linear model for microarray data (LIMMA) algorithm were used to determine hub genes. Then, Metascape database, DAVID database, and STRING database were used to annotate and visualize the gene ontology (GO) analysis, KEGG pathway enrichment analysis, and PPI network analysis of differentially expressed genes (DEGs). Finally, the TFs and miRNAs were predicted by using online tools, such as PASTAA and miRDB. Results. 20,484 differentially expressed genes related to atrial fibrillation were obtained through the analysis of left and right atrial tissue samples of GSE115574 gene chip, and 1,009 were with statistical significance, including 45 upregulated genes and 964 downregulated genes. And the hub genes implicated in AF of NPC2, ODC1, SNAP29, LAPTM5, ST8SIA5, and FCGR3B were screened. Finally, the main regulators of targeted candidate biomarkers and microRNAs, EIF5A2, HIF1A, ZIC2, ELF1, and STAT2, were found in this study. Conclusion. These hub genes, NPC2, ODC1, SNAP29, LAPTM5, ST8SIA5, and FCGR3B, are important for the development of VAF, and their enrichment pathways and TFs elucidate the involved molecular mechanisms and assist in the validation of drug targets.