Parkinson disease (PD) progresses relentlessly and affects approximately 4% of the population aged over 80 years old. It is difficult to diagnose in its early stages. The purpose of our study is to identify molecular biomarkers for PD initiation using a computational bioinformatics analysis of gene expression. We downloaded the gene expression profile of PD from Gene Expression Omnibus and identified differentially coexpressed genes (DCGs) and dysfunctional pathways in PD patients compared to controls. Besides, we built a regulatory network by mapping the DCGs to known regulatory data between transcription factors (TFs) and target genes and calculated the regulatory impact factor of each transcription factor. As the results, a total of 1004 genes associated with PD initiation were identified. Pathway enrichment of these genes suggests that biological processes of protein turnover were impaired in PD. In the regulatory network, HLF, E2F1 and STAT4 were found have altered expression levels in PD patients. The expression levels of other transcription factors, NKX3-1, TAL1, RFX1 and EGR3, were not found altered. However, they regulated differentially expressed genes. In conclusion, we suggest that HLF, E2F1 and STAT4 may be used as molecular biomarkers for PD; however, more work is needed to validate our result.

MicroRNAs are increasingly reported as tumour suppressors that regulate gene expression after transcription. Our results demonstrated that miR‐4295 is overexpression in glioma tissues and its level is significantly correlated with clinical stage. We also found that miR‐4295 inhibited the cell G0/G1 arrest and apoptosis leading to promoted cell proliferation and activity. The murine modelling study revealed that female nude mice injected with U87/anti‐miR‐4295 exhibit subcutaneous tumours in the right groin. Compared with anti‐NC, the tumour volume was significantly decreased in anti‐miR‐4295 treatment group. Furthermore, we confirmed miR‐4295 mediates the expression of RUNX3 by targeting its 3′untranslation region. In addition, N‐myc protein also could bind to the promoter of pri‐miR‐4295 and inhibit the expression of RUNX3 in glioma cells. These results validate a pathogenetic role of a miR‐4295 in gliomas and establish a potentially regulatory and signalling pathway involving N‐myc/miR‐4295/RUNX3 in gliomas.

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