Purpose. To mine miR expression in glioma based on the Gene Expression Omnibus (GEO) database and to explore its effects on biological functions. Methods. Differentially expressed miRs in glioma-related chips were found out based on the GEO database. Fifty patients with glioma treated in our hospital from February 2012 to July 2013 (observation group, OG) and a further 50 healthy people undergoing physical examinations (control group, CG) were enrolled. miR-873-5p expression in serum and in U87, T98G, U251, LN-229, and HEK-293T cells was tested by qRT-PCR. T98G and U251 cells were transfected with miR-873-5p-mimics and miR-NC sequences. The expression in the two cells was also tested by qRT-PCR. The proliferation, invasion, and apoptosis of the transfected cells were, respectively, tested by MTT assay, Transwell, and flow cytometry. The patients were followed up for 5 years to observe their survival. Results. miR-873-5p expression in OG was remarkably higher than that in CG ( p < 0.001 ). miR-873-5p was closely correlated with the tumor diameter, lymph node metastasis, and TNM staging of the patients ( p < 0.05 ). According to the plotted receiver operating characteristic (ROC) curves, the areas under the curves (AUCs) of miR-873-5p for diagnosing the disease, tumor diameter, lymph node metastasis, and TNM staging were 0.842, 0.706, 0.865, and 0.793, respectively. The 5-year and recurrence-free survival rates in the low expression group were lower than those in the high expression group. According to multivariate Cox regression analysis, tumor diameter, lymph node metastasis, and miR-873-5p were independent prognostic factors for the disease. After transfection, compared with those in the miR-NC group, T98G and U251 cells in the miR-873-5p-mimic group had remarkably higher miR-873-5p expression ( p < 0.05 ), remarkably lower proliferation and invasion rates ( p < 0.05 ), and a remarkably higher apoptotic rate ( p < 0.05 ). Conclusions. miR-873-5p can inhibit glioma cells to proliferate and invade, and promote their apoptosis, so it is expected to become a potential diagnostic index and therapeutic target for glioma.

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Parkinson’s disease (PD) is a common neurological disorder that causes quiescent tremors, motor delays, depression, and sleep disturbances. Existing treatments can only improve symptoms, not stop progression or cure the disease, but effective treatments can significantly improve patients’ quality of life. There is growing evidence that chromatin regulatory proteins (CRs) are involved in a variety of biological processes, including inflammation, apoptosis, autophagy, and proliferation. But the relationship of chromatin regulators in Parkinson’s disease has not been studied. Therefore, we aim to investigate the role of CRs in the pathogenesis of Parkinson’s disease. We collected 870 chromatin regulatory factors from previous studies and downloaded data on patients with PD from the GEO database. 64 differentially expressed genes were screened, the interaction network was constructed and the key genes with the top 20 scores were calculated. Then we discussed its correlation with the immune function of PD. Finally, we screened potential drugs and miRNAs. Five genes related to the immune function of PD, BANF1, PCGF5, WDR5, RYBP and BRD2, were obtained by using the absolute value of correlation greater than 0.4. And the disease prediction model showed good predictive efficiency. We also screened 10 related drugs and 12 related miRNAs, which provided a reference for the treatment of PD. BANF1, PCGF5, WDR5, RYBP and BRD2 are related to the immune process of Parkinson’s disease and can predict the occurrence of Parkinson’s disease, which is expected to become a new target for the diagnosis and treatment of Parkinson’s disease.