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LINC01018 and SMIM25 sponged miR-182-5p in endometriosis revealed by the ceRNA network construction
Li Jiang1, Mengmeng Zhang1, Sixue Wang1
1Department of Obstetrics and Gynecology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, P.R. China.
Abstract:
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.
Insights
This study reveals a competitive endogenous RNA (ceRNA) network in endometriosis, highlighting the interaction between long non-coding RNAs, microRNAs, and messenger RNAs. Key molecules like hsa-miR-182-5p, LINC01018, and CHL1 are implicated in inflammation and endometriosis development.
Area of Science:
- Molecular Biology
- Genomics
- Reproductive Medicine
Background:
- Endometriosis (EMs) is a complex gynecological disorder.
- The roles of long non-coding RNA (lncRNA), microRNA (miRNA), and messenger RNA (mRNA) interactions in EMs are not fully understood.
- Competitive endogenous RNA (ceRNA) networks regulate gene expression and are implicated in various diseases.
Purpose of the Study:
- To explore the lncRNA-miRNA-mRNA interactions within a ceRNA network in endometriosis.
- To identify key regulatory molecules and pathways involved in the pathogenesis of EMs.
- To investigate the potential diagnostic and therapeutic targets for endometriosis.
Main Methods:
- Differential expression analysis of RNA-sequencing data from ectopic (EC) and eutopic (EU) endometrium.
- Construction and analysis of a ceRNA network.
- Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, and protein-protein interaction (PPI) analyses.
- Validation of differentially expressed molecules and correlation analysis.
- Gene Set Enrichment Analysis (GSEA) to explore functional pathways.
Main Results:
- A ceRNA network was constructed, comprising differentially expressed miRNAs (DEmiRs), lncRNAs (DELs), and genes (DEGs).
- The ceRNA network was significantly associated with inflammation-related pathways.
- hsa-miR-182-5p, LINC01018, SMIM25, and CHL1 were identified as key molecules, with hsa-miR-182-5p negatively correlated with its targets.
- High expression of LINC01018, SMIM25, and CHL1, and low expression of hsa-miR-182-5p, were linked to activated inflammation pathways in eutopic endometrium.
Conclusions:
- The identified ceRNA network provides insights into the molecular mechanisms underlying endometriosis.
- hsa-miR-182-5p, LINC01018, and SMIM25 may play crucial roles in sponging hsa-miR-182-5p and upregulating downstream genes like CHL1, promoting endometriosis development.
- These findings suggest potential therapeutic targets for endometriosis based on ceRNA regulatory pathways.
