Long noncoding RNA TUG1 regulates degradation of chondrocyte extracellular matrix via miR-320c/MMP-13 axis in osteoarthritis

Osteoarthritis (OA) is a common chronic joint disease. This study aimed to explore the function of long noncoding RNA taurine-upregulated gene 1 (TUG1) in the progression and initiation of OA. Levels of TUG1, microRNA-320c (miR-320c) and fucosyltransferase 4 (FUT4) were examined via quantitative rev...

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Autores principales:	Han Hu, Liu Lijuan
Formato:	article
Lenguaje:	EN
Publicado:	De Gruyter 2021
Materias:	osteoarthritis tug1 mir-320c fut4 il-1β Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/d6957fb54a584f4c835ccd270c6cba90
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spelling	oai:doaj.org-article:d6957fb54a584f4c835ccd270c6cba902021-12-05T14:10:41ZLong noncoding RNA TUG1 regulates degradation of chondrocyte extracellular matrix via miR-320c/MMP-13 axis in osteoarthritis2391-541210.1515/biol-2021-0037https://doaj.org/article/d6957fb54a584f4c835ccd270c6cba902021-04-01T00:00:00Zhttps://doi.org/10.1515/biol-2021-0037https://doaj.org/toc/2391-5412Osteoarthritis (OA) is a common chronic joint disease. This study aimed to explore the function of long noncoding RNA taurine-upregulated gene 1 (TUG1) in the progression and initiation of OA. Levels of TUG1, microRNA-320c (miR-320c) and fucosyltransferase 4 (FUT4) were examined via quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide and flow cytometry assays were used to detect cell viability and apoptosis, respectively. The expression of relative proteins was measured using Western blot. The interaction between miR-320c and TUG1 or FUT4 was confirmed utilizing dual-luciferase reporter and RNA immunoprecipitation assays. In this study, levels of TUG1 and FUT4 were distinctly upregulated, but miR-320c level significantly decreased in OA tissues and chondrocytes derived from OA tissues as well as in IL-1β-stimulated C28/I2 cells. Mechanically, TUG1 sponged miR-320c and miR-320c targeted FUT4. In addition, TUG1 knockdown accelerated cell proliferation and repressed apoptosis and extracellular matrix (ECM) degradation in IL-1β-induced C28/I2 cells, whereas these effects of TUG1 deletion were rescued by either miR-320c inhibitor or FUT4 upregulation. Meanwhile, TUG1 sponged miR-320c to regulate FUT4 expression in IL-1β-induced C28/I2 cells. Collectively, TUG1 modulated cell proliferation, apoptosis and ECM degradation in IL-1β-induced C28/I2 cells via the miR-320c/FUT4 axis, providing a new insight into the OA treatment.Han HuLiu LijuanDe Gruyterarticleosteoarthritistug1mir-320cfut4il-1βBiology (General)QH301-705.5ENOpen Life Sciences, Vol 16, Iss 1, Pp 384-394 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	osteoarthritis tug1 mir-320c fut4 il-1β Biology (General) QH301-705.5
spellingShingle	osteoarthritis tug1 mir-320c fut4 il-1β Biology (General) QH301-705.5 Han Hu Liu Lijuan Long noncoding RNA TUG1 regulates degradation of chondrocyte extracellular matrix via miR-320c/MMP-13 axis in osteoarthritis
description	Osteoarthritis (OA) is a common chronic joint disease. This study aimed to explore the function of long noncoding RNA taurine-upregulated gene 1 (TUG1) in the progression and initiation of OA. Levels of TUG1, microRNA-320c (miR-320c) and fucosyltransferase 4 (FUT4) were examined via quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide and flow cytometry assays were used to detect cell viability and apoptosis, respectively. The expression of relative proteins was measured using Western blot. The interaction between miR-320c and TUG1 or FUT4 was confirmed utilizing dual-luciferase reporter and RNA immunoprecipitation assays. In this study, levels of TUG1 and FUT4 were distinctly upregulated, but miR-320c level significantly decreased in OA tissues and chondrocytes derived from OA tissues as well as in IL-1β-stimulated C28/I2 cells. Mechanically, TUG1 sponged miR-320c and miR-320c targeted FUT4. In addition, TUG1 knockdown accelerated cell proliferation and repressed apoptosis and extracellular matrix (ECM) degradation in IL-1β-induced C28/I2 cells, whereas these effects of TUG1 deletion were rescued by either miR-320c inhibitor or FUT4 upregulation. Meanwhile, TUG1 sponged miR-320c to regulate FUT4 expression in IL-1β-induced C28/I2 cells. Collectively, TUG1 modulated cell proliferation, apoptosis and ECM degradation in IL-1β-induced C28/I2 cells via the miR-320c/FUT4 axis, providing a new insight into the OA treatment.
format	article
author	Han Hu Liu Lijuan
author_facet	Han Hu Liu Lijuan
author_sort	Han Hu
title	Long noncoding RNA TUG1 regulates degradation of chondrocyte extracellular matrix via miR-320c/MMP-13 axis in osteoarthritis
title_short	Long noncoding RNA TUG1 regulates degradation of chondrocyte extracellular matrix via miR-320c/MMP-13 axis in osteoarthritis
title_full	Long noncoding RNA TUG1 regulates degradation of chondrocyte extracellular matrix via miR-320c/MMP-13 axis in osteoarthritis
title_fullStr	Long noncoding RNA TUG1 regulates degradation of chondrocyte extracellular matrix via miR-320c/MMP-13 axis in osteoarthritis
title_full_unstemmed	Long noncoding RNA TUG1 regulates degradation of chondrocyte extracellular matrix via miR-320c/MMP-13 axis in osteoarthritis
title_sort	long noncoding rna tug1 regulates degradation of chondrocyte extracellular matrix via mir-320c/mmp-13 axis in osteoarthritis
publisher	De Gruyter
publishDate	2021
url	https://doaj.org/article/d6957fb54a584f4c835ccd270c6cba90
work_keys_str_mv	AT hanhu longnoncodingrnatug1regulatesdegradationofchondrocyteextracellularmatrixviamir320cmmp13axisinosteoarthritis AT liulijuan longnoncodingrnatug1regulatesdegradationofchondrocyteextracellularmatrixviamir320cmmp13axisinosteoarthritis
_version_	1718371868444983296

Long noncoding RNA TUG1 regulates degradation of chondrocyte extracellular matrix via miR-320c/MMP-13 axis in osteoarthritis

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