The current study intended to explore the interaction of the long non-coding RNA (lncRNA), microRNA (miRNA), and messenger RNA (mRNA) under the background of competitive endogenous RNA (ceRNA) network in endometriosis (EMs). The differentially expressed miRNAs (DEmiRs), differentially expressed lncRNA (DELs), and differentially expressed genes (DEGs) between EMs ectopic (EC) and eutopic (EU) endometrium based on three RNA-sequencing datasets (GSE105765, GSE121406, and GSE105764) were identified, which were used for the construction of ceRNA network. Then, DEGs in the ceRNA network were performed with Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, and protein-protein interaction (PPI) analysis. Besides, the DEmiRs in the ceRNA network were validated in GSE124010. And the target DELs and DEGs of verified DEmiRs were validated in GSE86534. The correlation of verified DEmiRs, DEGs, and DELs was explored. Moreover, gene set enrichment analysis (GSEA) was applied to investigate the function of verified DEmiRs, DEGs, and DELs. Overall, 1352 DEGs and 595 DELs from GSE105764, along with 27 overlapped DEmiRs between GSE105765 and GSE121406, were obtained. Subsequently, a ceRNA network, including 11 upregulated and 16 downregulated DEmiRs, 7 upregulated and 13 downregulated DELs, 48 upregulated and 46 downregulated DEGs, was constructed. The GO and KEGG pathway analysis showed that this ceRNA network probably was associated with inflammation-related pathways. Furthermore, hsa-miR-182-5p and its target DELs (LINC01018 and SMIM25) and DEGs (BNC2, CHL1, HMCN1, PRDM16) were successfully verified in the validation analysis. Besides, hsa-miR-182-5p was significantly negatively correlated with these target DELs and DEGs. The GSEA analysis implied that high expression of LINC01018, SMIM25, and CHL1, and low expression of hsa-miR-182-5p would activate inflammation-related pathways in endometriosis EU samples.

LINC01018 and SMIM25 might sponge hsa-miR-182-5p to upregulate downstream genes such as CHL1 to promote the development of endometriosis.

目前的研究旨在探索在竞争性内源性RNA（ceRNA）网络背景下子宫内膜异位症（EMs）中长链非编码RNA（lncRNA）、微小RNA（miRNA）和信使RNA（mRNA）的相互作用。基于三个RNA测序数据集（GSE105765、GSE121406和GSE105764），EMs异位（EC）和在位（EU）子宫内膜之间的差异表达miRNA（DEmiRs）、差异表达lncRNA（DELs）和差异表达基因（DEGs）分别为鉴定，用于构建ceRNA网络。然后，使用基因本体论（GO）、京都基因和基因组百科全书（KEGG）途径和蛋白质-蛋白质相互作用（PPI）分析对ceRNA网络中的DEG进行分析。此外，ceRNA 网络中的 DEmiRs 在 GSE124010 中得到验证。经验证的 DEmiRs 的目标 DEL 和 DEG 在 GSE86534 中得到验证。探讨了经验证的 DEmiR、DEG 和 DEL 的相关性。此外，还应用基因集富集分析 (GSEA) 来研究经验证的 DEmiR、DEG 和 DEL 的功能。总的来说，获得了来自 GSE105764 的 1352 个 DEG 和 595 个 DEL，以及 GSE105765 和 GSE121406 之间的 27 个重叠的 DEmiR。随后，构建了一个 ceRNA 网络，包括 11 个上调和 16 个下调的 DEmiR、7 个上调和 13 个下调的 DEL、48 个上调和 46 个下调的 DEG。GO 和 KEGG 通路分析表明，该 ceRNA 网络可能与炎症相关通路有关。此外，hsa-miR-182-5p 及其目标 DEL（LINC01018 和 SMIM25）和 DEG（BNC2、CHL1、HMCN1、PRDM16) 在验证分析中被成功验证。此外，hsa-miR-182-5p 与这些目标 DEL 和 DEG 呈显着负相关。GSEA 分析表明，LINC01018、SMIM25 和 CHL1 的高表达和 hsa-miR-182-5p 的低表达将激活子宫内膜异位症 EU 样本中的炎症相关通路。

LINC01018 和 SMIM25 可能会海绵 hsa-miR-182-5p 上调 CHL1 等下游基因，从而促进子宫内膜异位症的发展。