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MicroRNA-98 acts as a tumor suppressor in hepatocellular carcinoma via targeting SALL4
MicroRNAs (miRs) are involved in the development and progression of hepatocellular carcinoma (HCC), but the regulatory mechanism of miR-98 in HCC still remains unclear. Here we found that miR-98 was significantly downregulated in HCC tissues compared to matched adjacent normal tissues (ANTs). Low mi...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5342035/ https://www.ncbi.nlm.nih.gov/pubmed/27677076 http://dx.doi.org/10.18632/oncotarget.12190 |
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author | Zhou, Wuyuan Zou, Benkui Liu, Lisheng Cui, Kai Gao, Jie Yuan, Shuanghu Cong, Ning |
author_facet | Zhou, Wuyuan Zou, Benkui Liu, Lisheng Cui, Kai Gao, Jie Yuan, Shuanghu Cong, Ning |
author_sort | Zhou, Wuyuan |
collection | PubMed |
description | MicroRNAs (miRs) are involved in the development and progression of hepatocellular carcinoma (HCC), but the regulatory mechanism of miR-98 in HCC still remains unclear. Here we found that miR-98 was significantly downregulated in HCC tissues compared to matched adjacent normal tissues (ANTs). Low miR-98 expression was associated with tumor size, metastasis, portal vein tumor embolus, and poor overall survival. Ectopic expression of miR-98 decreased the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of HCC cells. SALL4 was identified as a novel target of miR-98, and the protein expression of SALL4 was inhibited by miR-98 in HCC cells. Overexpression of SALL4 reversed the suppressive effects of miR-98 on the malignant phenotypes of HCC cells. Besides, SALL4, upregulated in HCC tissues compared to the matched ANTs, was inversely correlated to the miR-98 levels in HCC tissues. In addition, overexpression of miR-98 markedly suppressed the tumor growth as well as tumor-induced death in nude mice. In summary, miR-98 plays a suppressive role in the proliferation, migration, invasion and EMT of HCC cells, partly at least, via directly inhibition of SALL4. Therefore, the miR-98/SALL4 axis may become a promising therapeutic target for HCC. |
format | Online Article Text |
id | pubmed-5342035 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-53420352017-03-27 MicroRNA-98 acts as a tumor suppressor in hepatocellular carcinoma via targeting SALL4 Zhou, Wuyuan Zou, Benkui Liu, Lisheng Cui, Kai Gao, Jie Yuan, Shuanghu Cong, Ning Oncotarget Research Paper MicroRNAs (miRs) are involved in the development and progression of hepatocellular carcinoma (HCC), but the regulatory mechanism of miR-98 in HCC still remains unclear. Here we found that miR-98 was significantly downregulated in HCC tissues compared to matched adjacent normal tissues (ANTs). Low miR-98 expression was associated with tumor size, metastasis, portal vein tumor embolus, and poor overall survival. Ectopic expression of miR-98 decreased the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of HCC cells. SALL4 was identified as a novel target of miR-98, and the protein expression of SALL4 was inhibited by miR-98 in HCC cells. Overexpression of SALL4 reversed the suppressive effects of miR-98 on the malignant phenotypes of HCC cells. Besides, SALL4, upregulated in HCC tissues compared to the matched ANTs, was inversely correlated to the miR-98 levels in HCC tissues. In addition, overexpression of miR-98 markedly suppressed the tumor growth as well as tumor-induced death in nude mice. In summary, miR-98 plays a suppressive role in the proliferation, migration, invasion and EMT of HCC cells, partly at least, via directly inhibition of SALL4. Therefore, the miR-98/SALL4 axis may become a promising therapeutic target for HCC. Impact Journals LLC 2016-09-22 /pmc/articles/PMC5342035/ /pubmed/27677076 http://dx.doi.org/10.18632/oncotarget.12190 Text en Copyright: © 2016 Zhou et al. http://creativecommons.org/licenses/by/3.0/ 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 Zhou, Wuyuan Zou, Benkui Liu, Lisheng Cui, Kai Gao, Jie Yuan, Shuanghu Cong, Ning MicroRNA-98 acts as a tumor suppressor in hepatocellular carcinoma via targeting SALL4 |
title | MicroRNA-98 acts as a tumor suppressor in hepatocellular carcinoma via targeting SALL4 |
title_full | MicroRNA-98 acts as a tumor suppressor in hepatocellular carcinoma via targeting SALL4 |
title_fullStr | MicroRNA-98 acts as a tumor suppressor in hepatocellular carcinoma via targeting SALL4 |
title_full_unstemmed | MicroRNA-98 acts as a tumor suppressor in hepatocellular carcinoma via targeting SALL4 |
title_short | MicroRNA-98 acts as a tumor suppressor in hepatocellular carcinoma via targeting SALL4 |
title_sort | microrna-98 acts as a tumor suppressor in hepatocellular carcinoma via targeting sall4 |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5342035/ https://www.ncbi.nlm.nih.gov/pubmed/27677076 http://dx.doi.org/10.18632/oncotarget.12190 |
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