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Identification of endometriosis-associated genes and pathways based on bioinformatic analysis.

ABSTRACT:

Abstract

Endometriosis is associated with dysmenorrhea, chronic pelvic pain, and infertility. The specific mechanism of endometriosis remains unclear. The aim of this study was to apply a bioinformatics approach to reveal related pathways or genes involved in the development of endometriosis.The gene expression profiles of GSE25628, GSE5108, and GSE7305 were downloaded from the gene expression omnibus (GEO) database. Differentially expressed gene (DEG) analysis was performed using GEO2R. The database for annotation, visualization, and integrated discovery (DAVID) was utilized to analyze the functional enrichment, gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) pathway of the differentially expressed genes. A protein-protein interaction (PPI) network was constructed and module analysis was performed using search tool for the retrieval of interacting genes and cytoscape.A total of 119 common differentially expressed genes were extracted, consisting of 51 downregulated genes and 68 upregulated genes. The enriched functions and pathways of the DEGs and hub genes include DNA strand separation, cellular proliferation, degradation of the extracellular matrix, encoding of smooth muscle myosin as a major contractile protein, exiting the proliferative cycle and entering quiescence, growth regulation, and implication in a wide variety of biological processes.A bioinformatics approach combined with cell experiments in this study revealed that identifying DEGs and hub genes leads to better understanding of the molecular mechanisms underlying the progression of endometriosis, and efficient biomarkers underlying this pathway need to be further investigated.

SUBMITTER: Wang T

PROVIDER: S-EPMC8270630 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background: Endometriosis is a common gynecological disorder with high rates of infertility and pelvic pain. However, its pathogenesis and diagnostic biomarkers remain unclear. This study aimed to elucidate potential hub genes and key pathways associated with endometriosis in ectopic endometrium (EC) and eutopic endometrium (EU). Material and Method: EC and EU-associated microarray datasets were obtained from the gene expression omnibus (GEO) database. Gene set enrichment analysis was performed to obtain further biological insight into the EU and EC-associated genes. Weighted gene co-expression network analysis (WGCNA) was performed to find clinically significant modules of highly-correlated genes. The hub genes that belong to both the weighted gene co-expression network and protein-protein interaction (PPI) network were identified using a Venn diagram. Results: We obtained EC and EU-associated microarray datasets GSE7305 and GSE120103. Genes in the EC were mainly enriched in the immune response and immune cell trafficking, and genes in the EU were mainly enriched in stress response and steroid hormone biosynthesis. PPI networks and weighted gene co-expression networks were constructed. An EC-associated blue module and an EU-associated magenta module were identified, and their function annotations revealed that hormone receptor signaling or inflammatory microenvironments may promote EU passing through the oviducts and migrating to the ovarian surfaces, and adhesion and immune correlated genes may induce the successful ectopic implantation of the endometrium (EC). Twelve hub genes in the EC and sixteen hub genes in the EU were recognized and further validated in independent datasets. Conclusion: Our study identified, for the first time, the hub genes and enrichment pathways in the EC and EU using WGCNA, which may provide a comprehensive understanding of the pathogenesis of endometriosis and have important clinical implications for the treatment and diagnosis of endometriosis.

Project description:Lung cancer is the world's most common malignancies and ranks first among all cancer-related deaths. Lung adenocarcinoma (LUAD) is the most frequent histological type in lung cancer. Its pathogenesis has not yet been fully elucidated, so it is of great significance to explore related genes for elucidating the molecular mechanism involved in occurrence and development of LUAD.To explore the crucial genes associated with LUAD development and progression, microarray datasets GSE7670, GSE10072, and GSE31547 were acquired from the Gene Expression Omnibus (GEO) database. R language Limma package was adopted to screen the differentially expressed genes (DEGs). The clusterProfiler package was used for enrichment analysis and annotation of the Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genome (KEGG) pathways for DEGs. The Search Tool for the Retrieval of Interacting Genes database (STRING) was used to construct the protein interaction network for DEGs, while Cytoscape was adopted to visualize it. The functional module was screened with Cytoscape's MCODE (The Molecular Complex Detection) plugin. The crucial genes associated with LUAD were identified by cytoHubba plugin. Kaplan-Meier plotter online tool was used to perform survival analysis of the hub gene.Three hundred twenty-one DEGs in total were screened, of which 105 were upregulated and 216 were downregulated. It was found that some GO terms and pathways (e.g., collagen trimer, extracellular structure organization, heparin binding, complement and coagulation cascades, malaria, protein digestion and absorption, and PPAR signaling pathway) were considerably enriched in DEGs. UBE2C, TOP2A, RRM2, CDC20, CCNB2, KIAA0101, BUB1B, TPX2, PRC1, and CDK1 were identified as crucial genes. Survival analysis showed that the overexpression of UBE2C, TOP2A, RRM2, CDC20, CCNB2, KIAA0101, BUB1B, TPX2, and PRC1 significantly reduced the overall survival of LUAD patients. One of the crucial genes: UBE2C was validated by immunohistochemistry to be upregulated in LUAD tissues.This study screened out potential biomarkers of LUAD, providing a theoretical basis for elucidating the pathogenesis and evaluating the prognosis of LUAD.

Project description:PurposeNeuropathic pain is a complex chronic condition occurring post-nervous system damage. The transcriptional reprogramming of injured dorsal root ganglia (DRGs) drives neuropathic pain. However, few comparative analyses using high-throughput platforms have investigated uninjured DRG in neuropathic pain, and potential interactions among differentially expressed genes (DEGs) and pathways were not taken into consideration. The aim of this study was to identify changes in genes and pathways associated with neuropathic pain in uninjured L4 DRG after L5 spinal nerve ligation (SNL) by using bioinformatic analysis.Materials and methodsThe microarray profile GSE24982 was downloaded from the Gene Expression Omnibus database to identify DEGs between DRGs in SNL and sham rats. The prioritization for these DEGs was performed using the Toppgene database followed by gene ontology and pathway enrichment analyses. The relationships among DEGs from the protein interactive perspective were analyzed using protein-protein interaction (PPI) network and module analysis. Real-time polymerase chain reaction (PCR) and Western blotting were used to confirm the expression of DEGs in the rodent neuropathic pain model.ResultsA total of 206 DEGs that might play a role in neuropathic pain were identified in L4 DRG, of which 75 were upregulated and 131 were downregulated. The upregulated DEGs were enriched in biological processes related to transcription regulation and molecular functions such as DNA binding, cell cycle, and the FoxO signaling pathway. Ctnnb1 protein had the highest connectivity degrees in the PPI network. The in vivo studies also validated that mRNA and protein levels of Ctnnb1 were upregulated in both L4 and L5 DRGs.ConclusionThis study provides insight into the functional gene sets and pathways associated with neuropathic pain in L4 uninjured DRG after L5 SNL, which might promote our understanding of the molecular mechanisms underlying the development of neuropathic pain.

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Identification of endometriosis-associated genes and pathways based on bioinformatic analysis.

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