miR-338-5p Regulates the Viability, Proliferation, Apoptosis and Migration of Rheumatoid Arthritis Fibroblast-Like Synoviocytes by Targeting NFAT5
Abstract Background/Aims: MicroRNAs (miRNAs) have been reported to be involved in Rheumatoid arthritis (RA) pathogenesis and prognosis. However, little is known about the disease mechanism in RA. Here, we aim to investigate the potential association between miR-338-5p and NFAT5 in RA. Methods: Aberr...
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| Veröffentlicht in: | Cellular physiology and biochemistry 2018-01, Vol.49 (3), p.899-910 |
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| creator | Guo, Ting Ding, Hao Jiang, Hui Bao, Nirong Zhou, Liwu Zhao, Jianning |
| description | Abstract
Background/Aims: MicroRNAs (miRNAs) have been reported to be involved in Rheumatoid arthritis (RA) pathogenesis and prognosis. However, little is known about the disease mechanism in RA. Here, we aim to investigate the potential association between miR-338-5p and NFAT5 in RA. Methods: Aberrant expression of miR-338-5p in RA tissues and rheumatoid arthritis fibroblast-like synoviocytes (RAFLSs) compared to the normal were determined by RT-qPCR. Cell viability was determined using the CCK-8 assay, and cell apoptosis was analyzed via Annexin V-FITC/PI double staining and was detected using flow cytometry. The targeted relationship was determined by TargetScan database and dual luciferase reporter gene assay. Results: Upregulation of miR-338-5p facilitated the proliferation, migration, invasion and induced G0/G1 arrest of RAFLSs while miR-338-5p inhibitor functioned oppositely. Nuclear factor of activated T-cells 5 (NFAT5) was confirmed as a downstream target of miR-338-5p which expression was directly suppressed by miR-338-5p. Overexpression of NFAT5 attenuated the proliferation and metastasis of RAFLSs and those changes could be rescued by co-transfection of miR-338-5p. Conclusion: miR-338-5p promotes RAFLS’s viability and proliferation, migration by targeting NFAT5, suggesting a novel therapeutic strategy for RA. |
| doi_str_mv | 10.1159/000493222 |
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Background/Aims: MicroRNAs (miRNAs) have been reported to be involved in Rheumatoid arthritis (RA) pathogenesis and prognosis. However, little is known about the disease mechanism in RA. Here, we aim to investigate the potential association between miR-338-5p and NFAT5 in RA. Methods: Aberrant expression of miR-338-5p in RA tissues and rheumatoid arthritis fibroblast-like synoviocytes (RAFLSs) compared to the normal were determined by RT-qPCR. Cell viability was determined using the CCK-8 assay, and cell apoptosis was analyzed via Annexin V-FITC/PI double staining and was detected using flow cytometry. The targeted relationship was determined by TargetScan database and dual luciferase reporter gene assay. Results: Upregulation of miR-338-5p facilitated the proliferation, migration, invasion and induced G0/G1 arrest of RAFLSs while miR-338-5p inhibitor functioned oppositely. Nuclear factor of activated T-cells 5 (NFAT5) was confirmed as a downstream target of miR-338-5p which expression was directly suppressed by miR-338-5p. Overexpression of NFAT5 attenuated the proliferation and metastasis of RAFLSs and those changes could be rescued by co-transfection of miR-338-5p. Conclusion: miR-338-5p promotes RAFLS’s viability and proliferation, migration by targeting NFAT5, suggesting a novel therapeutic strategy for RA.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000493222</identifier><identifier>PMID: 30184542</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>3' Untranslated Regions ; Adult ; Angiogenesis ; Antagomirs - metabolism ; Apoptosis ; Arthritis, Rheumatoid - metabolism ; Arthritis, Rheumatoid - pathology ; Base Sequence ; Cancer ; Cell cycle ; Cell Movement ; Cell Proliferation ; Cells, Cultured ; Chemokines ; Cytokines ; Female ; Fibroblasts ; G1 Phase Cell Cycle Checkpoints ; Gene expression ; Humans ; Joint surgery ; Kinases ; Male ; MicroRNAs ; MicroRNAs - antagonists & inhibitors ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Middle Aged ; MiR-338-5p ; NFAT5 ; Original Paper ; Pathogenesis ; RAFLSs ; Rheumatoid arthritis ; Roles ; Sequence Alignment ; Synoviocytes - cytology ; Synoviocytes - metabolism ; Transcription Factors - chemistry ; Transcription Factors - genetics ; Transcription Factors - metabolism</subject><ispartof>Cellular physiology and biochemistry, 2018-01, Vol.49 (3), p.899-910</ispartof><rights>2018 The Author(s). Published by S. Karger AG, Basel</rights><rights>2018 The Author(s). Published by S. Karger AG, Basel.</rights><rights>2018 The Author(s). Published by S. Karger AG, Basel . Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the associated terms available at: https://uk.sagepub.com/en-gb/eur/reusing-open-access-and-sage-choice-content</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-9d916c6d6b6f062554a47e7c61c9ae3332e1d82632cf50bfd8be9678e983563d3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,861,2096,27616,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30184542$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Ting</creatorcontrib><creatorcontrib>Ding, Hao</creatorcontrib><creatorcontrib>Jiang, Hui</creatorcontrib><creatorcontrib>Bao, Nirong</creatorcontrib><creatorcontrib>Zhou, Liwu</creatorcontrib><creatorcontrib>Zhao, Jianning</creatorcontrib><title>miR-338-5p Regulates the Viability, Proliferation, Apoptosis and Migration of Rheumatoid Arthritis Fibroblast-Like Synoviocytes by Targeting NFAT5</title><title>Cellular physiology and biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Abstract
Background/Aims: MicroRNAs (miRNAs) have been reported to be involved in Rheumatoid arthritis (RA) pathogenesis and prognosis. However, little is known about the disease mechanism in RA. Here, we aim to investigate the potential association between miR-338-5p and NFAT5 in RA. Methods: Aberrant expression of miR-338-5p in RA tissues and rheumatoid arthritis fibroblast-like synoviocytes (RAFLSs) compared to the normal were determined by RT-qPCR. Cell viability was determined using the CCK-8 assay, and cell apoptosis was analyzed via Annexin V-FITC/PI double staining and was detected using flow cytometry. The targeted relationship was determined by TargetScan database and dual luciferase reporter gene assay. Results: Upregulation of miR-338-5p facilitated the proliferation, migration, invasion and induced G0/G1 arrest of RAFLSs while miR-338-5p inhibitor functioned oppositely. Nuclear factor of activated T-cells 5 (NFAT5) was confirmed as a downstream target of miR-338-5p which expression was directly suppressed by miR-338-5p. Overexpression of NFAT5 attenuated the proliferation and metastasis of RAFLSs and those changes could be rescued by co-transfection of miR-338-5p. Conclusion: miR-338-5p promotes RAFLS’s viability and proliferation, migration by targeting NFAT5, suggesting a novel therapeutic strategy for RA.</description><subject>3' Untranslated Regions</subject><subject>Adult</subject><subject>Angiogenesis</subject><subject>Antagomirs - metabolism</subject><subject>Apoptosis</subject><subject>Arthritis, Rheumatoid - metabolism</subject><subject>Arthritis, Rheumatoid - pathology</subject><subject>Base Sequence</subject><subject>Cancer</subject><subject>Cell cycle</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cells, Cultured</subject><subject>Chemokines</subject><subject>Cytokines</subject><subject>Female</subject><subject>Fibroblasts</subject><subject>G1 Phase Cell Cycle Checkpoints</subject><subject>Gene expression</subject><subject>Humans</subject><subject>Joint surgery</subject><subject>Kinases</subject><subject>Male</subject><subject>MicroRNAs</subject><subject>MicroRNAs - antagonists & inhibitors</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Middle Aged</subject><subject>MiR-338-5p</subject><subject>NFAT5</subject><subject>Original Paper</subject><subject>Pathogenesis</subject><subject>RAFLSs</subject><subject>Rheumatoid arthritis</subject><subject>Roles</subject><subject>Sequence Alignment</subject><subject>Synoviocytes - cytology</subject><subject>Synoviocytes - metabolism</subject><subject>Transcription Factors - chemistry</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DOA</sourceid><recordid>eNpt0ctv0zAcB_AIgdgYHLgjZGkXJi3gR_w6lorCpAJTKVwjv9K6S-NgO0j9N_YXk5LRA-Lk18dfP35F8RLBtwhR-Q5CWEmCMX5UnKMKo1JyLh6PfYhoKaTgZ8WzlHZwHHKJnxZnBCJR0QqfF_d7vyoJESXtwcpthlZll0DeOvDDK-1bnw_X4DaG1jcuquxDdw1mfehzSD4B1Vnw2W-mBRAasNq6Ya9y8BbMYt5Gn0e18DoG3aqUy6W_c-DboQu_fDCH41H6ANYqblz23QZ8WczW9HnxpFFtci8e2ovi--LDev6pXH79eDOfLUtTMZJLaSVihlmmWQMZprRSFXfcMGSkcoQQ7JAVmBFsGgp1Y4V2knHhpCCUEUsuipsp1wa1q_vo9yoe6qB8_WcixE2tYvamdTWjHNEKQaFxUxnmNHHEcIqF0tZARsesN1NWH8PPwaVc730yrm1V58KQaowgJBXCFR_p5T90F4bYjS8dFeJIQgKP6mpSJoaUomtOF0SwPha9PhV9tK8fEge9d_Yk_1Z5BK8mcHf86XgCp_2X_12e376fRN3bhvwGxCa6Ug</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Guo, Ting</creator><creator>Ding, Hao</creator><creator>Jiang, Hui</creator><creator>Bao, Nirong</creator><creator>Zhou, Liwu</creator><creator>Zhao, Jianning</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20180101</creationdate><title>miR-338-5p Regulates the Viability, Proliferation, Apoptosis and Migration of Rheumatoid Arthritis Fibroblast-Like Synoviocytes by Targeting NFAT5</title><author>Guo, Ting ; Ding, Hao ; Jiang, Hui ; Bao, Nirong ; Zhou, Liwu ; Zhao, Jianning</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-9d916c6d6b6f062554a47e7c61c9ae3332e1d82632cf50bfd8be9678e983563d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>3' Untranslated Regions</topic><topic>Adult</topic><topic>Angiogenesis</topic><topic>Antagomirs - metabolism</topic><topic>Apoptosis</topic><topic>Arthritis, Rheumatoid - metabolism</topic><topic>Arthritis, Rheumatoid - pathology</topic><topic>Base Sequence</topic><topic>Cancer</topic><topic>Cell cycle</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cells, Cultured</topic><topic>Chemokines</topic><topic>Cytokines</topic><topic>Female</topic><topic>Fibroblasts</topic><topic>G1 Phase Cell Cycle Checkpoints</topic><topic>Gene expression</topic><topic>Humans</topic><topic>Joint surgery</topic><topic>Kinases</topic><topic>Male</topic><topic>MicroRNAs</topic><topic>MicroRNAs - antagonists & inhibitors</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Middle Aged</topic><topic>MiR-338-5p</topic><topic>NFAT5</topic><topic>Original Paper</topic><topic>Pathogenesis</topic><topic>RAFLSs</topic><topic>Rheumatoid arthritis</topic><topic>Roles</topic><topic>Sequence Alignment</topic><topic>Synoviocytes - cytology</topic><topic>Synoviocytes - metabolism</topic><topic>Transcription Factors - chemistry</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guo, Ting</creatorcontrib><creatorcontrib>Ding, Hao</creatorcontrib><creatorcontrib>Jiang, Hui</creatorcontrib><creatorcontrib>Bao, Nirong</creatorcontrib><creatorcontrib>Zhou, Liwu</creatorcontrib><creatorcontrib>Zhao, Jianning</creatorcontrib><collection>Karger Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular physiology and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, Ting</au><au>Ding, Hao</au><au>Jiang, Hui</au><au>Bao, Nirong</au><au>Zhou, Liwu</au><au>Zhao, Jianning</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-338-5p Regulates the Viability, Proliferation, Apoptosis and Migration of Rheumatoid Arthritis Fibroblast-Like Synoviocytes by Targeting NFAT5</atitle><jtitle>Cellular physiology and biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>49</volume><issue>3</issue><spage>899</spage><epage>910</epage><pages>899-910</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Abstract
Background/Aims: MicroRNAs (miRNAs) have been reported to be involved in Rheumatoid arthritis (RA) pathogenesis and prognosis. However, little is known about the disease mechanism in RA. Here, we aim to investigate the potential association between miR-338-5p and NFAT5 in RA. Methods: Aberrant expression of miR-338-5p in RA tissues and rheumatoid arthritis fibroblast-like synoviocytes (RAFLSs) compared to the normal were determined by RT-qPCR. Cell viability was determined using the CCK-8 assay, and cell apoptosis was analyzed via Annexin V-FITC/PI double staining and was detected using flow cytometry. The targeted relationship was determined by TargetScan database and dual luciferase reporter gene assay. Results: Upregulation of miR-338-5p facilitated the proliferation, migration, invasion and induced G0/G1 arrest of RAFLSs while miR-338-5p inhibitor functioned oppositely. Nuclear factor of activated T-cells 5 (NFAT5) was confirmed as a downstream target of miR-338-5p which expression was directly suppressed by miR-338-5p. Overexpression of NFAT5 attenuated the proliferation and metastasis of RAFLSs and those changes could be rescued by co-transfection of miR-338-5p. Conclusion: miR-338-5p promotes RAFLS’s viability and proliferation, migration by targeting NFAT5, suggesting a novel therapeutic strategy for RA.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>30184542</pmid><doi>10.1159/000493222</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 3' Untranslated Regions Adult Angiogenesis Antagomirs - metabolism Apoptosis Arthritis, Rheumatoid - metabolism Arthritis, Rheumatoid - pathology Base Sequence Cancer Cell cycle Cell Movement Cell Proliferation Cells, Cultured Chemokines Cytokines Female Fibroblasts G1 Phase Cell Cycle Checkpoints Gene expression Humans Joint surgery Kinases Male MicroRNAs MicroRNAs - antagonists & inhibitors MicroRNAs - genetics MicroRNAs - metabolism Middle Aged MiR-338-5p NFAT5 Original Paper Pathogenesis RAFLSs Rheumatoid arthritis Roles Sequence Alignment Synoviocytes - cytology Synoviocytes - metabolism Transcription Factors - chemistry Transcription Factors - genetics Transcription Factors - metabolism |
| title | miR-338-5p Regulates the Viability, Proliferation, Apoptosis and Migration of Rheumatoid Arthritis Fibroblast-Like Synoviocytes by Targeting NFAT5 |
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