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Keywords {🔍}

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Topics {✒️}

mir-338-3p-gls-glutamine metabolic axis large-scale clip-seq data mir-338-3p-mediated flss-ra apoptosis predicted neat1-mir-338-3p association neat1-mir-338-3p-gls axis promoted h2o2-induced apoptosis flss-ra effectively restored predicted neat1-mir-338-3p interaction streptavidin-coupled agarose beads mir-410-3p/yyy1 axis [13] mir-410-3p/yy1 axis neat1-mediated glutamine metabolism neat1 sponges mir-338-3p mir-338-3p-gls pathway h2o2-induced flss dysfunction promoted flss-ra dysfunction neat1-mediated cellular metabolism mir-38-3p induces dysfunction mir-338-3p markedly blocked apoptosis-inducing agents based mir-338-3p binding sites analyzing mirna–lncrna interactions article download pdf pmir-report luciferase vector neat1-regulated glutamine metabolism mir-338-3p directly targets mirna-338-3p-mediated regulation xiao-yun guo mir-338-3p target candidates remove background dye incubating biotin-labeled control dual-luciferase assay system protein-rna interaction networks flss-ra exhibits features validate cell-based conclusions full access qrt-pcr cycling conditions related subjects biotin-labeled scramble control flss-ra lacking neat1 lncrna neat1 regulates lncrna neat1 pathway hong-jun li privacy choices/manage cookies promotes glutamine metabolism underlying molecular mechanisms human flss-ra compared clinical research center rna-rna complexes flss-ra cell lysates

Schema {🗺️}

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         headline:Inhibition of lncRNA NEAT1 induces dysfunction of fibroblast-like synoviocytes in rheumatoid arthritis via miRNA-338-3p-mediated regulation of glutamine metabolism
         description:Rheumatoid arthritis (RA) is a systemic chronic autoimmune disease; cellular glutamine metabolism in fibroblast-like synoviocytes (FLSs) of RA was known to be essential for RA pathogenesis and progression. NEAT1, a long non-coding RNA, functions as an oncogene in diverse cancers. The exact roles and molecular mechanisms of NEAT1 in fibroblast-like synoviocytes (FLSs) of RA patients are unknown. Expression of NEAT1 and miR-338-3p was measured by qRT-PCR. lncRNA-miRNA and miRNA-mRNA interactions were predicted from starBase and validated by RNA pull-down and luciferase assay. The glutamine metabolism of FLSs was evaluated by glutamine uptake and glutaminase activity. Cell death in FLSs in response to H2O2 was assessed by MTT and Annexin V assays. NEAT1 was significantly upregulated, and miR-338-3p was significantly downregulated in FLSs from RA patients compared to normal FLSs. Silencing of NEAT1 and overexpression of miR-338-3p suppressed glutamine metabolism in FLSs-RA and promoted H2O2-induced apoptosis. Bioinformatics analysis showed that NEAT1 sponges miR-338-3p to form competing endogenous RNA (ceRNAs), which was verified by RNA pull-down assay and luciferase assay FLSs-RA had an increased rate of glutamine metabolism compared to normal FLSs increased compared to normal FLSs. The results confirmed that GLS (Glutaminase), a key enzyme in glutamine metabolism, is a direct target of miR-338-3p in FLSs-RA. miR-338-3p inhibition of glutamine metabolism was verified by rescue experiments verified. Finally, restoration of miR-338-3p in FLSs-RA expressing NEAT1 overcomes NEAT1-promoted glutamine metabolism and resistance to apoptosis. This study reveals the essential role and molecular targets of NEAT1-regulated glutamine metabolism and FLSs-RA dysfunction in fibroblast-like synoviocytes of RA and indicates that blocking the molecular pathway via non-coding RNAs may be beneficial for RA patients.
         datePublished:2022-09-01T00:00:00Z
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            Fibroblast-like synoviocytes (FLSs)
            lncRNA
            NEAT1
            miR-338-3p
            Glutamine metabolism
            Orthopedics
            Surgical Orthopedics
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      headline:Inhibition of lncRNA NEAT1 induces dysfunction of fibroblast-like synoviocytes in rheumatoid arthritis via miRNA-338-3p-mediated regulation of glutamine metabolism
      description:Rheumatoid arthritis (RA) is a systemic chronic autoimmune disease; cellular glutamine metabolism in fibroblast-like synoviocytes (FLSs) of RA was known to be essential for RA pathogenesis and progression. NEAT1, a long non-coding RNA, functions as an oncogene in diverse cancers. The exact roles and molecular mechanisms of NEAT1 in fibroblast-like synoviocytes (FLSs) of RA patients are unknown. Expression of NEAT1 and miR-338-3p was measured by qRT-PCR. lncRNA-miRNA and miRNA-mRNA interactions were predicted from starBase and validated by RNA pull-down and luciferase assay. The glutamine metabolism of FLSs was evaluated by glutamine uptake and glutaminase activity. Cell death in FLSs in response to H2O2 was assessed by MTT and Annexin V assays. NEAT1 was significantly upregulated, and miR-338-3p was significantly downregulated in FLSs from RA patients compared to normal FLSs. Silencing of NEAT1 and overexpression of miR-338-3p suppressed glutamine metabolism in FLSs-RA and promoted H2O2-induced apoptosis. Bioinformatics analysis showed that NEAT1 sponges miR-338-3p to form competing endogenous RNA (ceRNAs), which was verified by RNA pull-down assay and luciferase assay FLSs-RA had an increased rate of glutamine metabolism compared to normal FLSs increased compared to normal FLSs. The results confirmed that GLS (Glutaminase), a key enzyme in glutamine metabolism, is a direct target of miR-338-3p in FLSs-RA. miR-338-3p inhibition of glutamine metabolism was verified by rescue experiments verified. Finally, restoration of miR-338-3p in FLSs-RA expressing NEAT1 overcomes NEAT1-promoted glutamine metabolism and resistance to apoptosis. This study reveals the essential role and molecular targets of NEAT1-regulated glutamine metabolism and FLSs-RA dysfunction in fibroblast-like synoviocytes of RA and indicates that blocking the molecular pathway via non-coding RNAs may be beneficial for RA patients.
      datePublished:2022-09-01T00:00:00Z
      dateModified:2022-09-01T00:00:00Z
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         Rheumatoid arthritis (RA)
         Fibroblast-like synoviocytes (FLSs)
         lncRNA
         NEAT1
         miR-338-3p
         Glutamine metabolism
         Orthopedics
         Surgical Orthopedics
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      name:Lu Lu
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      name:Department of Breast Medical Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin’s Clinical Research Center for Cancer, Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin Medical University, Ministry of Education, Tianjin, People’s Republic of China
      name:Department of Rheumatology and Immunology, The Second Hospital of Tianjin Medical University, Tianjin, People’s Republic of China
      name:Department of Nephrology, The Second Hospital of Tianjin Medical University, Tianjin, People’s Republic of China
      name:Department of Pharmacy, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin’s Clinical Research Center for Cancer, Tianjin, People’s Republic of China
      name:Department of Rheumatology and Immunology, Tianjin Medical University General Hospital, Tianjin, People’s Republic of China

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