Mining and analyzing key genes of androgenic alopecia based on public database

Objective To explore the potential molecular mechanism of androgenetic alopecia (AGA) by using bioinformatics methods.

Methods The gene chip data sets (GSE45512, GSE36169) were downloaded from the gene expression database of the public data platform of the National Center for Biotechnology Information, and the GEO2R online analysis tool was used to analyze them and obtain their respective differential expressed genes (DEGs). GO and KEGG enrichment analysis of differential genes were performed using DAVID online tool. The protein network of DEGs was constructed using STRING database, calculated by Cytohubba plug-in in Cytoscape software, and ranked from high to low according to MCC score. According to the score results, the top three genes were selected as Hub genes and further verified in clinical samples.

Results The DEGs related to AGA were selected from the two chip data sets and further intersected. A total of 29 DEGs were obtained, of which 13 were up-regulated and 16 were down-regulated. GO enrichment analysis of 29 DEGs indicated that biological processes such as protein processing and amyloid metabolism were related to the pathogenesis of the disease. KEGG enrichment analysis suggested that dilated cardiomyopathy, Alzheimer's disease and other related pathways were associated with it. The protein network was constructed using STRING database. As a result, Cytoscape software was uploaded to screen out three key genes with the highest scores: MYH11, TPM4 and SORBS1 according to MCC scores, which were taken as Hub genes. The subsequent validation of Hub gene in clinical samples suggested that compared with healthy control group, the expression of MYH11 in patients was significantly down-regulated (P < 0.01), while the expression of TPM4 and SORBS1 in patients was significantly up-regulated (P < 0.01).

Conclusions The key genes TPM4, SORBS1 and MYH11 in AGA are screened by bioinformatics method, which brings new ideas for the pathogenesis of AGA and has potential value for exploring new treatment schemes.