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miR-211 suppresses hepatocellular carcinoma by downregulating SATB2

Dysregulation of microRNAs (miRs) is involved in carcinogenesis. Deregulation of miR-211 has recently been observed in many tumors, but its function in hepatocellular carcinoma (HCC) is still unknown. Here we found that miR-211 was decreased in HCC cancer tissues compared with adjacent normal tissue...

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Autores principales: Jiang, Guixing, Cui, Yunfu, Yu, Xin, Wu, Zhengrong, Ding, Guoping, Cao, Liping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4496230/
https://www.ncbi.nlm.nih.gov/pubmed/25888635
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author Jiang, Guixing
Cui, Yunfu
Yu, Xin
Wu, Zhengrong
Ding, Guoping
Cao, Liping
author_facet Jiang, Guixing
Cui, Yunfu
Yu, Xin
Wu, Zhengrong
Ding, Guoping
Cao, Liping
author_sort Jiang, Guixing
collection PubMed
description Dysregulation of microRNAs (miRs) is involved in carcinogenesis. Deregulation of miR-211 has recently been observed in many tumors, but its function in hepatocellular carcinoma (HCC) is still unknown. Here we found that miR-211 was decreased in HCC cancer tissues compared with adjacent normal tissues. We also found that overexpression of miR-211 repressed proliferation and invasion in HepG2 and SMMC7721 cells. Luciferase reporter assays and western blot indicated that special AT-rich sequence-binding protein-2 (SATB2), is a direct target of miR-211. The expression of SATB2 was upregulated in HCC cancer tissues and cell lines and miR-211 levels inversely correlated with SATB2 levels in HCC. Importantly, SATB2 rescued the miR-211-mediated inhibition of cell invasion and proliferation. Finally, reintroduction of miR-211 repressed tumor formation of HCC in xenograft mice. This study provides insights into molecular mechanisms that miR-211 contributed to HCC.
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spelling pubmed-44962302015-07-10 miR-211 suppresses hepatocellular carcinoma by downregulating SATB2 Jiang, Guixing Cui, Yunfu Yu, Xin Wu, Zhengrong Ding, Guoping Cao, Liping Oncotarget Research Paper Dysregulation of microRNAs (miRs) is involved in carcinogenesis. Deregulation of miR-211 has recently been observed in many tumors, but its function in hepatocellular carcinoma (HCC) is still unknown. Here we found that miR-211 was decreased in HCC cancer tissues compared with adjacent normal tissues. We also found that overexpression of miR-211 repressed proliferation and invasion in HepG2 and SMMC7721 cells. Luciferase reporter assays and western blot indicated that special AT-rich sequence-binding protein-2 (SATB2), is a direct target of miR-211. The expression of SATB2 was upregulated in HCC cancer tissues and cell lines and miR-211 levels inversely correlated with SATB2 levels in HCC. Importantly, SATB2 rescued the miR-211-mediated inhibition of cell invasion and proliferation. Finally, reintroduction of miR-211 repressed tumor formation of HCC in xenograft mice. This study provides insights into molecular mechanisms that miR-211 contributed to HCC. Impact Journals LLC 2015-03-25 /pmc/articles/PMC4496230/ /pubmed/25888635 Text en Copyright: © 2015 Jiang et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Jiang, Guixing
Cui, Yunfu
Yu, Xin
Wu, Zhengrong
Ding, Guoping
Cao, Liping
miR-211 suppresses hepatocellular carcinoma by downregulating SATB2
title miR-211 suppresses hepatocellular carcinoma by downregulating SATB2
title_full miR-211 suppresses hepatocellular carcinoma by downregulating SATB2
title_fullStr miR-211 suppresses hepatocellular carcinoma by downregulating SATB2
title_full_unstemmed miR-211 suppresses hepatocellular carcinoma by downregulating SATB2
title_short miR-211 suppresses hepatocellular carcinoma by downregulating SATB2
title_sort mir-211 suppresses hepatocellular carcinoma by downregulating satb2
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4496230/
https://www.ncbi.nlm.nih.gov/pubmed/25888635
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