{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cai Y"],"funding":["National Natural Science Foundation of China"],"pagination":["134"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6547523"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(1)"],"pubmed_abstract":["<h4>Background</h4>We previously found that high-mobility group box protein 1 (HMGB1) promoted cell proliferation, migration, invasion, and autophagy in rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS), but little is known about its regulatory mechanism. The aim of this study was to investigate the regulatory mechanism of HMGB1 at the posttranscription level.<h4>Methods</h4>Real-time qPCR, CCK-8 cell proliferation assay, transwell cell migration assay, enzyme-linked immunosorbent assay (ELISA), and western blotting were used in this study. The targeting relationship between miRNA and mRNA was presented by the luciferase reporter assay.<h4>Results</h4>MiR-449a was downregulated in RA synovial tissue and inhibited RA-FLS proliferation, migration, and IL-6 production. MiR-449a direc"],"journal":["Arthritis research & therapy"],"pubmed_title":["miR-449a inhibits cell proliferation, migration, and inflammation by regulating high-mobility group box protein 1 and forms a mutual inhibition loop with Yin Yang 1 in rheumatoid arthritis fibroblast-like synoviocytes."],"pmcid":["PMC6547523"],"funding_grant_id":["81772410","81271948","81601877"],"pubmed_authors":["Ren X","Xu L","Xu K","Xu P","Wang B","Guo Y","Yuan Q","Qiu Y","Zhu J","Cai Y","Jiang C","Sun J","Hu P"],"additional_accession":[]},"is_claimable":false,"name":"miR-449a inhibits cell proliferation, migration, and inflammation by regulating high-mobility group box protein 1 and forms a mutual inhibition loop with Yin Yang 1 in rheumatoid arthritis fibroblast-like synoviocytes.","description":"<h4>Background</h4>We previously found that high-mobility group box protein 1 (HMGB1) promoted cell proliferation, migration, invasion, and autophagy in rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS), but little is known about its regulatory mechanism. The aim of this study was to investigate the regulatory mechanism of HMGB1 at the posttranscription level.<h4>Methods</h4>Real-time qPCR, CCK-8 cell proliferation assay, transwell cell migration assay, enzyme-linked immunosorbent assay (ELISA), and western blotting were used in this study. The targeting relationship between miRNA and mRNA was presented by the luciferase reporter assay.<h4>Results</h4>MiR-449a was downregulated in RA synovial tissue and inhibited RA-FLS proliferation, migration, and IL-6 production. MiR-449a direc","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Jun","modification":"2025-05-18T11:02:09.048Z","creation":"2025-05-18T11:02:09.048Z"},"accession":"S-EPMC6547523","cross_references":{"pubmed":["31159863"],"doi":["10.1186/s13075-019-1920-0"]}}