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Objective To detect the expression levels of miR-7-5p and POLE4 in non-small cell lung cancer cells and their effect on cells proliferation, migration and invasion. Methods qRT-PCR was used to detect the relative expression levels of miR-7-5p and POLE4 mRNA in NSCLC tissues, adjacent tissues, tumor cells and human normal bronchial epithelial cells. Luciferase reporter gene was used for analyzing of the targeting relation between POLE4 and miR-7-5p in NSCLC cells. si-NC and si-POLE4 were transfected into SPC-A-1 cells as the si-NC group and si-POLE4 group, and the control group was set at the same time. MTT method, scratch test and Transwell test were used to detect cell proliferation, migration and invasion. Results The expression levels of miR-7-5p in NSCLC tissues and cells were reduced, and the expression levels of POLE4 were increased. miR-7-5p could target to combine with POLE4. After 72 hours of culture, the OD value in si-POLE4 group was significantly lower than those in the control group and si-NC group (P < 0.05). The migration rate and the number of transmembrane cells in the si-POLE4 group cultured for 48 hours were lower than those in the control group and the si-NC group (P < 0.05). Conclusion miR-7-5p may inhibit the proliferation, migration and invasion of non-small cell lung cancer cells by targeting POLE4.

With the participation of the existing treatment methods, the prognosis of advanced clear‐cell renal cell carcinoma (ccRCC) is poor. More evidence indicates the presence of methylation in ccRCC cancer cells, but there is a lack of studies on methylation‐driven genes in ccRCC. We analyzed the open data of ccRCC in The Cancer Genome Atlas database to obtain ccRCC‐related methylation‐driven genes, and then carried out pathway enrichment, survival, and joint survival analyses. More important, we deeply explored the correlation between differential methylation sites and the expression of these driving genes. Finally, we screened 29 methylation‐driven genes via MethylMix, of which six were significantly associated with the survival of ccRCC patients. This study demonstrated that the effect of hypermethylation or hypomethylation on prognosis is different, and the level of methylation of key methylation sites is associated with gene expression. We identified methylation‐driven genes independently predicting prognosis in ccRCC, which offers theoretical support in bioinformatics for the study of methylation in ccRCC and a new perspective for the epigenetic study of ccRCC. [ABSTRACT FROM AUTHOR]