Molecular basis of AR and STK11 genes associated pathogenesis via AMPK pathway and adipocytokine signalling pathway in the development of metabolic disorders in PCOS women

5Citations
Citations of this article
12Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Background: One of the most common hormonal disorders in women of reproductive age is polycystic ovary syndrome (PCOS). In recent years, it has been found that insulin resistance is a common metabolic abnormality in women with PCOS and leads to an elevated risk of type 2 diabetes mellitus. To explore the differentially expressed genes (DEGs) that regulate these kinds of metabolic risks in PCOS women, we chose the gene expression profile of GSE8157 from the gene expression omnibus (GEO) database. Results: Using the GEO2R tool, we identified a total of 339 DEGs between the case and the control sample groups. Gene ontology and Kyoto encyclopedia of gene and genome pathway enrichment analysis were subsequently conducted. High connectivity, betweenness centrality, bottleneck centrality, closeness centrality, and radiality measures were used to rank the ten hub genes. Furthermore, the overlap of these genes resulted in the development of two key genes, AR and STK11. The AMPK and adipocytokine signaling pathways are the two main pathways that these DEGs are involved. Conclusions: The backbone genes, hub genes and pathways identified would assist us in further exploring the molecular basis of developing risk of type 2 diabetes mellitus in PCOS women and thus provide diagnostic or therapeutic clues.

Cite

CITATION STYLE

APA

Gollapalli, P., Kumari, N. S., Shetty, P., & Gnanasekaran, T. S. (2022). Molecular basis of AR and STK11 genes associated pathogenesis via AMPK pathway and adipocytokine signalling pathway in the development of metabolic disorders in PCOS women. Beni-Suef University Journal of Basic and Applied Sciences, 11(1). https://doi.org/10.1186/s43088-022-00200-8

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free