ArticleJournal of clinical laboratory analysis2021
Influences of the lncRNA TUG1-miRNA-34a-5p network on fibroblast-like synoviocytes (FLSs) dysfunction in rheumatoid arthritis through targeting the lactate dehydrogenase A (LDHA).
Article in Journal of clinical laboratory analysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- The emerging role of lactate in skeletal homeostasis and disorders: Integrated mechanisms and translational opportunities.Journal of orthopaedic translation · 2026Review
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Immunometabolic reprogramming in rheumatoid arthritis: the epitranscriptomic role of N6-methyladenosine in innate and adaptive immunity.Frontiers in immunology · 2026Review
- Immunometabolic dysregulation in autoimmune rheumatic diseases: the central role of glycolytic reprogramming in pathogenesis and traditional Chinese medicine therapy.Frontiers in immunology · 2026Review
- Beta sitosterol inhibits the proliferation and migration of synoviocytes in rheumatoid arthritis via lactylation of GPI.Scientific reports · 2025Article
- Review
- The Role of Long Non-Coding RNA in Rheumatoid Arthritis.International journal of molecular sciences · 2025Review
- Metabolic reprogramming: the central mechanism driving inflammatory polarization in rheumatoid arthritis and the regulatory role of traditional Chinese medicine.Frontiers in immunology · 2025Review
- The Role and Mechanism of Protein Post‑Translational Modification in Rheumatoid Arthritis.Journal of inflammation research · 2025Review
- Role of miRNAs in Rheumatoid Arthritis Therapy.Cells · 2023Review
- Bovine tumor necrosis factor-alpha Increases IL-6, IL-8, and PGE2 in bovine fibroblast-like synoviocytes by metabolic reprogramming.Scientific reports · 2023Article
- Functional Relevance of the Long Intergenic Non-Coding RNA Regulator of Reprogramming (Linc-ROR) in Cancer Proliferation, Metastasis, and Drug Resistance.Non-coding RNA · 2023Review
- Bioinformatics analysis of microarray data to identify hub genes, as diagnostic biomarker of HELLP syndrome: System biology approach.The journal of obstetrics and gynaecology research · 2022Article
- Long Intergenic Noncoding RNAs Affect Biological Pathways Underlying Autoimmune and Neurodegenerative Disorders.Molecular neurobiology · 2022Review
- Lactylation, an emerging hallmark of metabolic reprogramming: Current progress and open challenges.Frontiers in cell and developmental biology · 2022Review
- Influences of the lncRNA TUG1-miRNA-34a-5p network on fibroblast-like synoviocytes (FLSs) dysfunction in rheumatoid arthritis through targeting the lactate dehydrogenase A (LDHA).Journal of clinical laboratory analysis · 2021Article
- Role of Lactate in Inflammatory Processes: Friend or Foe.Frontiers in immunology · 2021Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRheumatoid arthritis (RA) is a systemic and chronic inflammatory disease. The cellular glucose metabolism of fibroblast-like synoviocytes (FLSs) of RA has been revealed to be essential to the pathogenesis and development of RA. To date, the precise roles and molecular mechanisms of long noncoding RNA TUG1 in RA have not been elucidated.
methodsTUG1 and miR-34a-5p were detected by qRT-PCR. Interactions between lncRNA-miRNA and miRNA-mRNA were validated by RNA pull-down assay and luciferase assay. The glucose metabolism was evaluated by glucose uptake and extracellular acidification rate (ECAR). Cell viability was determined by MTT assay and Annexin V assay.
resultsTUG1 expression was significantly upregulated in synovial fibroblast-like synoviocytes (FLSs) compared with normal FLSs. Functional assays uncovered that silence of TUG1 suppressed FLSs-RA invasion, migration, glucose metabolism, and increased apoptosis. Bioinformatics analysis indicated that TUG1 interacted with miR-34a-5p. RNA pull-down assay and luciferase assay validated that TUG1 sponged miR-34a-5p in FLSs-RA. Overexpression of miR-34a-5p effectively inhibited glucose metabolism of FLSs-RA. Furthermore, the glucose metabolism of FLSs-RA was significantly elevated compared with normal FLSs. The glucose metabolism enzyme, LDHA, was directly targeted by miR-34a-5p in FLSs. Rescue experiments validated that the miR-34a-5p-inhibited glucose metabolism of FLSs-RA was through targeting LDHA. Finally, we showed restoration of miR-34a-5p in TUG1-overexpressing FLSs-RA successfully overcame the TUG1-promoted glucose metabolism and apoptosis resistance via targeting LDHA.
conclusionThe present study uncovered critical roles and molecular mechanisms underlying the TUG1-mediated glucose metabolism and apoptosis of FLSs-RA through modulating the miR-34a-5p-LDHA pathway in fibroblast-like synoviocytes of rheumatoid arthritis.
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