Persistent dysregulation of genes in the development of endometriosis

Abstract

Background: Endometriosis is a chronic condition that affects women of child-bearing age. Since the etiology and pathogenesis of endometriosis have not been fully elucidated, it is important to investigate the mechanisms that lead to the deterioration of endometriosis.Methods: In this study, the transcriptome data of patients with normal, mild, and severe endometriosis were examined using the GSE51981 dataset obtained from the Gene Expression Omnibus database. Short Time Series Expression Miner (STEM) was used to screen the genes with continuous expression disorder in the development process, and the core genes were identified by constructing a protein-protein interaction network. The molecular mechanisms of endometriosis were examined using enrichment analysis. Finally, the transcription factors that regulate the core genes were predicted and the comprehensive mechanisms involved in the development of endometriosis were examined.Results: A total of 3,472 differentially expressed genes were identified from the normal, mild, and severe endometriosis samples. These were allocated into 12 modules and HRAS, HSP90AA1, TGFB1, TP53, and UBC were selected as the core genes. Enrichment analysis showed that the genes in modules 6, 7, and 9 were significantly related to oxygen levels, metallic processes, and hormone levels, respectively. Transcription factor prediction analysis showed that TP53 regulates HRAS to participate in immune related signaling pathways. Drug prediction analysis identified 792 drugs that interact with the targeted core genes. Conclusions:This study explored the molecular mechanisms involved in the development of endometriosis and identified potential biomarkers of endometriosis. This data may provide novel targets and research directions for the diagnosis and treatment of endometriosis.

Evaluation of Proteasome and Immunoproteasome Levels in Plasma and Peritoneal Fluid in Patients with Endometriosis

“…In contrast to the proteasome, we did not observe a reduction in plasma immunoproteasome levels in mild endometriosis. The onset of endometriosis can be divided into two stages: an initial immune-dependent stage and a later stage in which estrogen signaling dominates [ 30 ]. More inflammatory markers are secreted in the early stages of endometriosis [ 31 ], including cytokines that stimulate immunoproteasome formation.…”