<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cai Y</submitter><funding>National Natural Science Foundation of China</funding><pagination>134</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6547523</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/h4>MiR-449a was downregulated in RA synovial tissue and inhibited RA-FLS proliferation, migration, and IL-6 production. MiR-449a direc</pubmed_abstract><journal>Arthritis research &amp; therapy</journal><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.</pubmed_title><pmcid>PMC6547523</pmcid><funding_grant_id>81772410</funding_grant_id><funding_grant_id>81271948</funding_grant_id><funding_grant_id>81601877</funding_grant_id><pubmed_authors>Ren X</pubmed_authors><pubmed_authors>Xu L</pubmed_authors><pubmed_authors>Xu K</pubmed_authors><pubmed_authors>Xu P</pubmed_authors><pubmed_authors>Wang B</pubmed_authors><pubmed_authors>Guo Y</pubmed_authors><pubmed_authors>Yuan Q</pubmed_authors><pubmed_authors>Qiu Y</pubmed_authors><pubmed_authors>Zhu J</pubmed_authors><pubmed_authors>Cai Y</pubmed_authors><pubmed_authors>Jiang C</pubmed_authors><pubmed_authors>Sun J</pubmed_authors><pubmed_authors>Hu P</pubmed_authors></additional><is_claimable>false</is_claimable><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.</name><description>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/h4>MiR-449a was downregulated in RA synovial tissue and inhibited RA-FLS proliferation, migration, and IL-6 production. MiR-449a direc</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Jun</publication><modification>2025-05-18T11:02:09.048Z</modification><creation>2025-05-18T11:02:09.048Z</creation></dates><accession>S-EPMC6547523</accession><cross_references><pubmed>31159863</pubmed><doi>10.1186/s13075-019-1920-0</doi></cross_references></HashMap>