Effects of CDKN2B-AS1 on cellular proliferation, invasion and AKT3 expression are attenuated by miR-424-5p in a model of ovarian endometriosis
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⤵ 12 in-corpus citations
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The lncRNA CDKN2B-AS1 promotes ovarian endometriosis cell proliferation and invasion, but its effects are suppressed by miR-424-5p, which also downregulates AKT3 expression.
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Abstract
RESEARCH QUESTION: Endometriosis is a common and complicated gynaecologic disease. Long non-coding RNA CDKN2B-AS1 plays a crucial role in the development and progression of several cancers. Whether CDKN2B-AS1 contributes to endometriosis, however, remains unknown.
DESIGN: Cellular proliferation, invasion and DNA synthesis abilities were assessed by CCK8, transwell and 5-ethynyle-2'-deoxyuridine assays. The expression of epithelial-mesenchymal transition markers and three isoforms of AKT was detected using Western blot. Real-time polymerase chain reaction was used to determine the relative expression levels of CDKN2B-AS1 and candidate miRNAs in ectopic, eutopic endometria and normal endometrial tissues. The relationship between CDKN2B-AS1 and miRNA was determined by luciferase reporter assays.
RESULTS: The relative expression level of CDKN2B-AS1 was up-regulated in eutopic and ectopic endometria. In endometrial stromal cells and Ishikawa cells, CDKN2B-AS1 overexpression promoted cellular proliferation and invasion, and increased the protein expression of vimentin but decreased the expression of E-cadherin. miR-424-5p was confirmed the target of CDKN2B-AS1 through bioinformatics tools and luciferase reporter assays. In addition, the enhanced effect of cellular phenotype of CDKN2B-AS1 overexpression was significantly attenuated by miR-424-5p overexpression. Furthermore, miR-424-5p was able to directly target AKT3 through luciferase reporter assay. Mechanistically, CDKN2B-AS1 acts as a ceRNA by sponging miR-424-5p and targets AKT3.
CONCLUSIONS: The cellular mechanism of CDKN2B-AS1 in endometriosis was confirmed; CDKN2B-AS1 may be a potential target for ovarian endometriosis therapy.
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Cited by (14)
- The hypoxia-epigenetics-ncRNA axis in endometriosis: from molecular cascades to self-sustaining pathogenic circuits 2026
- Immune-epigenetic-metabolic crosstalk: attempting to unravel the multidimensional mechanisms of immune evasion in endometriosis 2026
- Leveraging epigenetic aberrations in the pathogenesis of endometriosis: from DNA methylation to non-coding RNAs 2025
- A modern view of the problem of endometriosis from a genetic point of view (literature review) 2025
- Combined targeting of TCF7L1/2, PTEN, CDK6, and BCCIP by microRNA miR-29c-3p is associated with reduced invasion and proliferation of endometriotic cells 2025
- LINC01140/miR-200c-3p and LINC01550/miR-363-3p networks play pivotal role in orchestrating progression of endometriosis† 2025
- Novel Diagnostic Biomarker BST2 Identified by Integrated Transcriptomics Promotes the Development of Endometriosis via the TNF-α/NF-κB Signaling Pathway 2024
- Apparent lncRNAs involvement in pathogenesis of endometriosis 2024
- Linc-ROR Promotes EMT by Targeting miR-204-5p/SMAD4 in Endometriosis 2023
- [Lowered expression of CCN5 in endometriotic tissues promotes proliferation, migration and invasion of endometrial stromal cells] 2022
- Silencing of circ_0007299 suppresses proliferation, migration, and invasiveness and promotes apoptosis of ectopic endometrial stromal cells in endometriosis via miR-424-5p-dependent modulation of CREB1 2022
- A review of the effects of estrogen and epithelial-mesenchymal transformation on intrauterine adhesion and endometriosis 2022
- The Role of Long Non-Coding RNAs in Endometriosis 2021
- miR-424-5p Combined with miR-17-5p Has High Diagnostic Efficacy for Endometriosis 2021
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