WITHDRAWN: CD24 promotes the migration of eutopic endometrial stromal cells from endometriosis and relevant differentially expressed genes and signaling pathways

Abstract

<h2>ABSTRACT</h2><h3>Research question</h3> <b>:</b> What is the implication of aberrant CD24 expressions in endometriosis (EM) and the relevant mechanisms? <h3>Design</h3> <b>:</b> Thirty women with EM and twenty-seven women with other benign gynecological diseases, who underwent laparoscopy and hysteroscopy, were recruited in this study. The hEM15A cells were used in functional experiments <i>in vitro</i>. The microarray assay and bioinformatics analyses were performed to investigate the differentially expressed genes (DEGs) and signaling pathways regulated by CD24. <h3>Results</h3> <b>:</b> CD24 was expressed at significantly higher levels in eutopic endometrial (EU) tissues than in paired ectopic endometrial (EC) tissues from EM patients and normal endometrial (NE) tissues from controls. However, the CD24 expressions had no obvious relationships with clinical features such as age, infertility conditions, and menstrual cycle phase. Suppression of CD24 by small interfering RNAs in hEM15A cells impaired cell migration and reduced cytoskeletal filamentous actin (F-actin), but had no effects on cell apoptosis, cell cycle or cell viability. A total of 862 DEGs were identified between siCD24 and siNC, which consisted of 517 upregulated genes and 345 downregulated genes. The gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses for the DEGs mainly focused on the type I interferon signaling pathway and TGF-beta signaling pathway. Gene set enrichment analysis (GSEA) was also conducted. Furthermore, a protein-protein interaction (PPI) network and subnetwork were constructed to explore the hub modules and DEGs. <h3>Conclusions</h3> <b>:</b> This study provides a better understanding of the role of CD24 in EM.