ArticleJournal of cellular and molecular medicine2019
LncRNA MEG3 inhibits rheumatoid arthritis through miR-141 and inactivation of AKT/mTOR signalling pathway.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Research progress on serological indices and their clinical application in rheumatoid arthritis.Journal of clinical laboratory analysis · 2022Pooled it
- LncRNAs and IgA nephropathy: underlying molecular pathways and clinical applications.Clinical and experimental medicine · 2025Review
- The Challenges of Local Intra-Articular Therapy.Medicina (Kaunas, Lithuania) · 2024Review
- Long non-coding RNA MEG3 silencing weakens high glucose-induced mesangial cell injury by decreasing LIN28B expression by sponging and sequestering miR-23c.Kidney research and clinical practice · 2024Article
- Unveiling Novel Drug Targets and Emerging Therapies for Rheumatoid Arthritis: A Comprehensive Review.ACS pharmacology & translational science · 2024Review
- Roles of long noncoding RNAs in human inflammatory diseases.Cell death discovery · 2024Review
- Article
- Role of long non-coding RNA in inflammatory bowel disease.Frontiers in immunology · 2024Review
- Epigenetic Regulation of Autophagy in Bone Metabolism.Function (Oxford, England) · 2024Review
- Long noncoding RNA/circular RNA regulates competitive endogenous RNA networks in rheumatoid arthritis: molecular mechanisms and traditional Chinese medicine therapeutic significances.Annals of medicine · 2023Review
- Downregulation of BIRC2 hinders the progression of rheumatoid arthritis through regulating TRADD.Immunity, inflammation and disease · 2023Article
- Long noncoding RNA00324 is involved in the inflammation of rheumatoid arthritis by targeting miR-10a-5p via the NF-κB pathway.Immunity, inflammation and disease · 2023Article
- Inhibition of Cdc37 Ameliorates Arthritis in Collagen-Induced Arthritis Rats by Inhibiting Synoviocyte Proliferation and Migration Through the ERK Pathway.Inflammation · 2023Article
- Comprehensive overview of microRNA function in rheumatoid arthritis.Bone research · 2023Review
- MicroRNA-122-3p plays as the target of long non-coding RNA LINC00665 in repressing the progress of arthritis.Bioengineered · 2022Article
- Article
- lncRNA BZRAP1-AS1 alleviates rheumatoid arthritis by regulating miR-1286/COL5A2 axis.Immunity, inflammation and disease · 2022Article
- Article
- A review of current evidence about lncRNA MEG3: A tumor suppressor in multiple cancers.Frontiers in cell and developmental biology · 2022Review
- Functional Interactions Between lncRNAs/circRNAs and miRNAs: Insights Into Rheumatoid Arthritis.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is a chronic inflammation mediated by autoimmune responses. MEG3, a kind of long noncoding RNA (lncRNA), participates in cell proliferation in cancer tissues. However, the correlation between MEG3 and RA is yet unclear. Therefore, to clarify how MEG3 works in RA, we performed a series of experiments using RA samples. We found that MEG3 was downregulated in the fibroblast-like synoviocytes of RA patients (RA-FLS), in comparison with healthy subjects. MEG3 was also down-regulated evidently in lipopolysaccharide (LPS)-treated chondrocyte. As part of our experiments, MEG3 was overexpressed in chondrocyte by transfection with lentivirus containing sequences encoding MEG3. In addition, in presence of LPS, reductions were identified not only in the cell proliferation, but also in the generation of interleukin-23 (IL-23), which, however were reversed in the lentivirus (containing MEG3-encoding sequences)-transfected chondrocytes. Up-regulated MEG3 resulted in an increase the level of Ki67. Moreover, MEG3 was negatively correlated with miR-141, and miR-141 was up-regulated in LPS-treated chondrocyte. Inhibitory effects of MEG3 overexpression, mentioned above, were partially abolished by overexpressed miR-141. Further, animal experiment also showed the inhibitory effect of MEG3 in overexpression on the AKT/mTOR signaling pathway. In-vivoexperiments also showed that cell proliferation was facilitated by MEG3 overexpression with inhibited inflammation. In summary, the protective role of MEG3 in RA was proved to be exerted by the increase in the rate of proliferation, which might correlate to the regulatory role of miR-141 and AKT/mTOR signal pathway, suggesting that MEG3 holds great promise as a therapeutic strategy for RA.
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