Integrated Bioinformatics Analysis Reveals Function and Regulatory Network of miR-200b-3p in Endometriosis

Abstract EN

Objective.

MicroRNAs play vital roles in the development of endometriosis.

It is reported that miR-200b-3p is downregulated in endometriosis, although its mechanisms in this disease remain still unclear.

Therefore, the purpose of this study was to explore the function and potential regulatory network of miR-200b-3p in endometriosis through database analysis.

Methods.

The endometriosis gene expression profiles were downloaded from the GEO database to screen differentially expressed genes (DEGs).

The predicted and validated target genes of miR-200b-3p were obtained from miRWalk and miRTarBase database.

Then, a comparison was performed between miR-200b-3p target genes and DEGs.

GO enrichment and KEGG pathway analysis of the target genes was performed using clusterProfiler package.

STRING was used to predict the protein-protein interaction among the proteins encoded by the target genes.

Then, TransmiR, LncBase, StarBase, PROMO, and AnimalTFDB were employed to identify interactive transcription factors and lncRNAs of miR-200b-3p.

Results.

miR-200b-3p was associated with the transcription factors DNMT1, EZH2, HNF1B, JUN, MYB, ZEB1, and ZEB2 during the pathogenesis of endometriosis.

The downstream 110 target genes were involved in the biological processes of positive regulation of MAPK cascade, muscle cell proliferation, organ growth, vasculogenesis, and axon development.

KEGG analysis revealed that the main pathways related to miR-200b-3p were microRNAs in cancer, PI3K-Akt signaling pathway, colorectal cancer, and tight junction.

In addition, four lncRNAs such as MALAT1, NEAT1, SNHG22, and XIST interacted with miR-200b-3p and were associated with transcription factors FOXP3 and YY1.

Conclusion.

The predicted target genes and molecular regulatory network of miR-200b-3p in endometriosis not only revealed its biological function but also provided a valuable guideline for further research.