子宫内膜异位症
生物标志物
免疫系统
趋化因子
免疫学
生物
候选基因
医学
癌症研究
肿瘤科
基因
内科学
遗传学
作者
Lei Gan,Jiani Sun,Jing Sun
出处
期刊:PeerJ
[PeerJ]
日期:2022-03-30
卷期号:10: e13218-e13218
被引量:3
摘要
Endometriosis is a chronic systemic disease, whose classic symptoms are pelvic pain and infertility. This disease seriously reduces the life quality of patients. The pathogenesis, recognition and treatment of endometriosis is still unclear, and cannot be over emphasized. The aim of our study was to investigate the potential biomarker of endometriosis for the mechanism and treatment.Using GSE11691, GSE23339 and GSE5108 datasets, differentially expressed genes (DEGs) were identified between endometriosis and normal samples. The functions of DEGs were reflected by the analysis of gene ontology (GO), pathway enrichment and gene set enrichment analysis (GSEA). The LASSO regression model was performed to identify candidate biomarkers. The receiver operating characteristic curve (ROC) was used to evaluate discriminatory ability of candidate biomarkers. The predictive value of the markers in endometriosis were further validated in the GSE120103 dataset. Then, the expression level of biomarkers was detected by qRT-PCR and Western blot. Finally, the relationship between candidate biomarker expression and immune infiltration was estimated using CIBERSORT.A total of 42 genes were identified, which were mainly involved in cytokine-cytokine receptor interaction, systemic lupus erythematosus and chemokine signaling pathway. We confirmed PDLIM3 was a specific biomarker in endometriosis (AUC = 0.955) and validated in the GSE120103 dataset (AUC = 0.836). The mRNA and protein expression level of PDLIM3 in endometriosis tissue was significantly higher than normal. Immune cell infiltration analysis revealed that PDLIM3 was correlated with M2 macrophages, neutrophils, CD4+ memory resting T cells, gamma delta T cells, M1 Macrophages, resting mast cells, follicular helper T cells, activated NK cells, CD8+ T cells, regulatory T cells (Tregs), naive B cells, plasma cells and resting NK cells.
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