ArticleMolecular and cellular biochemistry2021
MiR-182 inhibits proliferation, migration, invasion and inflammation of endometrial stromal cells through deactivation of NF-κB signaling pathway in endometriosis.
Article in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 43 citations in OpenAlex.
- The interaction between inflammation and estrogen in adenomyosis : from molecular mechanisms to therapeutic strategies.Seminars in immunopathology · 2026Review
- Mechanistic insights into inflammatory cytokines in adenomyosis‑induced infertility (Review).International journal of molecular medicine · 2026Review
- Endometriosis as a Systemic and Complex Disease: Toward Phenotype-Based Classification and Personalized Therapy.International journal of molecular sciences · 2026Review
- Dysregulation of Key Biological Processes in Endometriosis Pathophysiology.Current molecular medicine · 2026Review
- Molecular mechanisms underlying the inhibition of cell migration and invasion in endometriosis: Advances in pharmacological research (Review).Biomedical reports · 2025Review
- Emerging biologic and clinical implications of miR-182-5p in gynecologic cancers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Neurotrimin, a neural adhesion molecule, expression in early and advanced stage endometriosis.Revista brasileira de ginecologia e obstetricia : revista da Federacao Brasileira das Sociedades de Ginecologia e Obstetricia · 2025Observational
- Update on the pathogenesis of endometriosis-related infertility based on contemporary evidence.Frontiers in endocrinology · 2025Review
- Unraveling pathogenesis, biomarkers and potential therapeutic agents for endometriosis associated with disulfidptosis based on bioinformatics analysis, machine learning and experiment validation.Journal of biological engineering · 2024Article
- mir-182-5p regulates all three phases of inflammation, proliferation, and remodeling during cutaneous wound healing.Archives of dermatological research · 2024Article
- Therapeutic Potential of Natural Resources Against Endometriosis: Current Advances and Future Perspectives.Drug design, development and therapy · 2024Review
- MicroRNAs in Endometriosis: Insights into Inflammation and Progesterone Resistance.International journal of molecular sciences · 2023Review
- The landscape of non-coding RNAs in the immunopathogenesis of Endometriosis.Frontiers in immunology · 2023Review
- Inhibition of miR-182-5p Targets FGF9 to Alleviate Osteoarthritis.Analytical cellular pathology (Amsterdam) · 2023Article
- Genome-wide post-transcriptional regulation of bovine mammary gland response to Streptococcus uberis.Journal of applied genetics · 2022Article
- Integrated bioinformatic analysis of dysregulated microRNA-mRNA co-expression network in ovarian endometriosis.Acta obstetricia et gynecologica Scandinavica · 2022Article
- An Update on the Multifaceted Role of NF-kappaB in Endometriosis.International journal of biological sciences · 2022Review
- Role of inflammation in benign gynecologic disorders: from pathogenesis to novel therapies†.Biology of reproduction · 2021Review
- Comprehensive Analysis of Correlations in the Expression of miRNA Genes and Immune Checkpoint Genes in Bladder Cancer Cells.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Endometriosis affects about 10-15% women for reproductive age, but it is not currently curable and the underlying etiology for this disease is still not clear. In the present study, functions and mechanisms of miR-182 and RELA in endometriosis were investigated. BAY 11-7082 was used to block NF-κB pathway. qRT-PCR, ELISA and western blot assays were employed to evaluate the expressions of miR-182 and RELA, inflammatory factors and epithelial-mesenchymal transition (EMT)-related markers, and activation of NF-κB pathway. MTT, wound healing or Transwell assays were used to evaluate the cell proliferation, migration and invasion capacities. Bioinformatic and dual-luciferase reporter assays were carried out to analyze the interaction between miR-182 and RELA. MiR-182 expression was decreased, while RELA was increased as developed from normal to eutopic and ectopic status, which was accompanied by upregulated inflammatory factors and EMT-related proteins. RELA was directly targeted by miR-182 in human endometrial stromal cells. Overexpression of RELA increased inflammation-associated and EMT-related markers expression, while miR-182 upregulation decreased the expression of these genes in a dose-dependent manner, which finally attenuated the proliferation, migration and invasion capacities of endometrial stromal cells through deactivation of NF-κB signaling pathway. Moreover, co-overexpression of RELA reversed the above effects induced by miR-182. In a word, miR-182 directly targeted RELA and inhibited proliferation, migration, invasion, EMT and inflammation of endometrial stromal cells through deactivation of NF-κB signaling pathway in endometriosis. These results provide new insights into the interaction between miR-182 and NF-κB pathway and their potential as therapeutic targets for treatment of endometriosis.
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Registered trials
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