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MicroRNA-613 represses lipogenesis in HepG2 cells by downregulating LXRα
BACKGROUND: MicroRNAs (miRNAs) emerge as new important regulators of lipid homeostasis by regulating corresponding genes. MiR-613 is a newly discovered microRNA, of which the biological function is unknown. A recent report has shown that miR-613 downregulates liver X receptor α (LXRα), a ligand-acti...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3605323/ https://www.ncbi.nlm.nih.gov/pubmed/23496987 http://dx.doi.org/10.1186/1476-511X-12-32 |
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author | Zhong, Dan Zhang, Yan Zeng, Yi-jun Gao, Min Wu, Geng-ze Hu, Chang-jiang Huang, Gang He, Feng-tian |
author_facet | Zhong, Dan Zhang, Yan Zeng, Yi-jun Gao, Min Wu, Geng-ze Hu, Chang-jiang Huang, Gang He, Feng-tian |
author_sort | Zhong, Dan |
collection | PubMed |
description | BACKGROUND: MicroRNAs (miRNAs) emerge as new important regulators of lipid homeostasis by regulating corresponding genes. MiR-613 is a newly discovered microRNA, of which the biological function is unknown. A recent report has shown that miR-613 downregulates liver X receptor α (LXRα), a ligand-activated nuclear receptor playing an important role in the regulation of lipid metabolism. The purpose of this study is to explore the effect and the molecular basis of miR-613 on lipogenesis in HepG2 cells. METHODS: HepG2 cells were transiently transfected with miR-613 mimic or control microRNA. Real time PCR, Western blot, Luciferase reporter assay and Oil Red O staining were employed to examine the expression of LXRα and its target genes involved in lipogenesis, binding site for miR-613 in 3(′)-untranslated region (3(′)-UTR) of LXRα mRNA and lipid droplet accumulation in the cells. RESULTS: MiR-613 dramatically suppressed the expression of LXRα and its target genes including sterol-regulatory element binding protein 1c (SREBP-1c), fatty acid synthase (FAS), carbohydrate responsive element-binding protein (ChREBP) and acetyl-CoA carboxylase (ACC). Reporter assay showed that miR-613 directly bound to 3(′)-UTR of LXRα mRNA. Moreover, miR-613 significantly repressed LXRα-induced lipid droplet accumulation in HepG2 cells. Ectopic expression of LXRα without 3(′)-UTR markedly attenuated the miR-613-mediated downregulation of LXRα’s target genes and LXRα-induced lipid droplet accumulation. CONCLUSIONS: MiR-613 suppresses lipogenesis by directly targeting LXRα in HepG2 cells, suggesting that miR-613 may serve as a novel target for regulating lipid homeostasis. |
format | Online Article Text |
id | pubmed-3605323 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-36053232013-03-23 MicroRNA-613 represses lipogenesis in HepG2 cells by downregulating LXRα Zhong, Dan Zhang, Yan Zeng, Yi-jun Gao, Min Wu, Geng-ze Hu, Chang-jiang Huang, Gang He, Feng-tian Lipids Health Dis Research BACKGROUND: MicroRNAs (miRNAs) emerge as new important regulators of lipid homeostasis by regulating corresponding genes. MiR-613 is a newly discovered microRNA, of which the biological function is unknown. A recent report has shown that miR-613 downregulates liver X receptor α (LXRα), a ligand-activated nuclear receptor playing an important role in the regulation of lipid metabolism. The purpose of this study is to explore the effect and the molecular basis of miR-613 on lipogenesis in HepG2 cells. METHODS: HepG2 cells were transiently transfected with miR-613 mimic or control microRNA. Real time PCR, Western blot, Luciferase reporter assay and Oil Red O staining were employed to examine the expression of LXRα and its target genes involved in lipogenesis, binding site for miR-613 in 3(′)-untranslated region (3(′)-UTR) of LXRα mRNA and lipid droplet accumulation in the cells. RESULTS: MiR-613 dramatically suppressed the expression of LXRα and its target genes including sterol-regulatory element binding protein 1c (SREBP-1c), fatty acid synthase (FAS), carbohydrate responsive element-binding protein (ChREBP) and acetyl-CoA carboxylase (ACC). Reporter assay showed that miR-613 directly bound to 3(′)-UTR of LXRα mRNA. Moreover, miR-613 significantly repressed LXRα-induced lipid droplet accumulation in HepG2 cells. Ectopic expression of LXRα without 3(′)-UTR markedly attenuated the miR-613-mediated downregulation of LXRα’s target genes and LXRα-induced lipid droplet accumulation. CONCLUSIONS: MiR-613 suppresses lipogenesis by directly targeting LXRα in HepG2 cells, suggesting that miR-613 may serve as a novel target for regulating lipid homeostasis. BioMed Central 2013-03-08 /pmc/articles/PMC3605323/ /pubmed/23496987 http://dx.doi.org/10.1186/1476-511X-12-32 Text en Copyright ©2013 Zhong et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Zhong, Dan Zhang, Yan Zeng, Yi-jun Gao, Min Wu, Geng-ze Hu, Chang-jiang Huang, Gang He, Feng-tian MicroRNA-613 represses lipogenesis in HepG2 cells by downregulating LXRα |
title | MicroRNA-613 represses lipogenesis in HepG2 cells by downregulating LXRα |
title_full | MicroRNA-613 represses lipogenesis in HepG2 cells by downregulating LXRα |
title_fullStr | MicroRNA-613 represses lipogenesis in HepG2 cells by downregulating LXRα |
title_full_unstemmed | MicroRNA-613 represses lipogenesis in HepG2 cells by downregulating LXRα |
title_short | MicroRNA-613 represses lipogenesis in HepG2 cells by downregulating LXRα |
title_sort | microrna-613 represses lipogenesis in hepg2 cells by downregulating lxrα |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3605323/ https://www.ncbi.nlm.nih.gov/pubmed/23496987 http://dx.doi.org/10.1186/1476-511X-12-32 |
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