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MicroRNA-3651 promotes the growth and invasion of hepatocellular carcinoma cells by targeting PTEN
BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in human worldwide. Evidence indicated that upregulation of microRNA-3651 (miR-3651) was observed in human HCC tissues. In this study, we explored the mechanisms by which miR-3651 regulated the proliferation, apopt...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6718252/ https://www.ncbi.nlm.nih.gov/pubmed/31695418 http://dx.doi.org/10.2147/OTT.S213705 |
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author | Zhao, Xinyang Song, Qilong Miao, Ge Zhu, Xinfeng |
author_facet | Zhao, Xinyang Song, Qilong Miao, Ge Zhu, Xinfeng |
author_sort | Zhao, Xinyang |
collection | PubMed |
description | BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in human worldwide. Evidence indicated that upregulation of microRNA-3651 (miR-3651) was observed in human HCC tissues. In this study, we explored the mechanisms by which miR-3651 regulated the proliferation, apoptosis and invasion of HCC. METHODS: The levels of miR-3651 in human HCC tissues were detected using qRT-PCR assay. In addition, transwell invasion and Western blot assay were conducted to detect cell invasion and apoptosis, respectively. Meanwhile, the dual-luciferase reporter assay was used to explore the interaction of miR-3651 and phosphate and tension homology deleted on chromsome ten (PTEN) in HCC. RESULTS: The levels of miR-3651 were upregulated in HCC tissues in comparison with the matched normal tissues. Overexpression of miR-3651 significantly promoted the proliferation and invasion of Huh-7 cells. In contrast, inhibition of miR-3651 markedly inhibited the proliferation and invasion of Huh-7 cells via promoting apoptosis. Moreover, downregulation of miR-3651 markedly inhibited tumor growth in vivo. Furthermore, bioinformatics analysis and luciferase reporter assay identified that PTEN was the directly binding target of miR-3651 in Huh-7 cells. Meanwhile, overexpression of miR-3651 obviously decreased the level of PTEN, and increased the expressions of p-p85 and p-Akt in Huh-7 cells. CONCLUSION: These results indicated that miR-3651 might act as a potential oncogene in HCC by targeting PTEN. Therefore, miR-3651 might be a novel therapeutic target for the treatment of HCC. |
format | Online Article Text |
id | pubmed-6718252 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-67182522019-11-06 MicroRNA-3651 promotes the growth and invasion of hepatocellular carcinoma cells by targeting PTEN Zhao, Xinyang Song, Qilong Miao, Ge Zhu, Xinfeng Onco Targets Ther Original Research BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in human worldwide. Evidence indicated that upregulation of microRNA-3651 (miR-3651) was observed in human HCC tissues. In this study, we explored the mechanisms by which miR-3651 regulated the proliferation, apoptosis and invasion of HCC. METHODS: The levels of miR-3651 in human HCC tissues were detected using qRT-PCR assay. In addition, transwell invasion and Western blot assay were conducted to detect cell invasion and apoptosis, respectively. Meanwhile, the dual-luciferase reporter assay was used to explore the interaction of miR-3651 and phosphate and tension homology deleted on chromsome ten (PTEN) in HCC. RESULTS: The levels of miR-3651 were upregulated in HCC tissues in comparison with the matched normal tissues. Overexpression of miR-3651 significantly promoted the proliferation and invasion of Huh-7 cells. In contrast, inhibition of miR-3651 markedly inhibited the proliferation and invasion of Huh-7 cells via promoting apoptosis. Moreover, downregulation of miR-3651 markedly inhibited tumor growth in vivo. Furthermore, bioinformatics analysis and luciferase reporter assay identified that PTEN was the directly binding target of miR-3651 in Huh-7 cells. Meanwhile, overexpression of miR-3651 obviously decreased the level of PTEN, and increased the expressions of p-p85 and p-Akt in Huh-7 cells. CONCLUSION: These results indicated that miR-3651 might act as a potential oncogene in HCC by targeting PTEN. Therefore, miR-3651 might be a novel therapeutic target for the treatment of HCC. Dove 2019-08-29 /pmc/articles/PMC6718252/ /pubmed/31695418 http://dx.doi.org/10.2147/OTT.S213705 Text en © 2019 Zhao et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Zhao, Xinyang Song, Qilong Miao, Ge Zhu, Xinfeng MicroRNA-3651 promotes the growth and invasion of hepatocellular carcinoma cells by targeting PTEN |
title | MicroRNA-3651 promotes the growth and invasion of hepatocellular carcinoma cells by targeting PTEN |
title_full | MicroRNA-3651 promotes the growth and invasion of hepatocellular carcinoma cells by targeting PTEN |
title_fullStr | MicroRNA-3651 promotes the growth and invasion of hepatocellular carcinoma cells by targeting PTEN |
title_full_unstemmed | MicroRNA-3651 promotes the growth and invasion of hepatocellular carcinoma cells by targeting PTEN |
title_short | MicroRNA-3651 promotes the growth and invasion of hepatocellular carcinoma cells by targeting PTEN |
title_sort | microrna-3651 promotes the growth and invasion of hepatocellular carcinoma cells by targeting pten |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6718252/ https://www.ncbi.nlm.nih.gov/pubmed/31695418 http://dx.doi.org/10.2147/OTT.S213705 |
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