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Interferon-α inhibits cell migration and invasion and induces the expression of antiviral proteins in Huh-7 cells transfected with hepatitis B virus X gene-expressing lentivirus
Hepatitis B virus (HBV) X protein (HBx) serves an important role in HBV infection and the development of HBV-related liver cancer. Interferon-α (IFN-α) is used to treat patients with HBV; however, the role of IFN-α in the development of HBV-related liver cancer remains unclear. The present study est...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5740601/ https://www.ncbi.nlm.nih.gov/pubmed/29285141 http://dx.doi.org/10.3892/etm.2017.5288 |
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author | Yang, Qian Li, Xiao-Peng Zhong, Yuan-Bin Xiang, Tian-Xin Zhang, Lun-Li |
author_facet | Yang, Qian Li, Xiao-Peng Zhong, Yuan-Bin Xiang, Tian-Xin Zhang, Lun-Li |
author_sort | Yang, Qian |
collection | PubMed |
description | Hepatitis B virus (HBV) X protein (HBx) serves an important role in HBV infection and the development of HBV-related liver cancer. Interferon-α (IFN-α) is used to treat patients with HBV; however, the role of IFN-α in the development of HBV-related liver cancer remains unclear. The present study established a new HBV-related liver cancer model (Huh-7-HBx) by transfecting the hepatoma cell line Huh-7, with HBx-expressing lentivirus. Following IFN-α treatment, cell viability, migration and invasion, as well as the expression of antiviral proteins in Huh-7-HBx, were subsequently determined. The results demonstrated that HBx-expressing lentivirus had no significant effect on cell viability but promoted the migration and invasion of Huh-7 cells. The expression of the antiviral genes IFN α and β receptor subunit 1 (IFNAR1), IFNAR2, IFN-stimulated gene factor 3, double-stranded RNA-activated protein kinase and ribonuclease L, was also increased. Following treatment of Huh-7-HBx cells with IFN-α, the expression of antiviral genes was increased at the level of transcription and translation, whereas cell migration and invasion was decreased. The present study suggests that IFN-α may attenuate the development of HBV-related liver cancer by reducing cell migration and invasion and promoting the expression of antiviral proteins. |
format | Online Article Text |
id | pubmed-5740601 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-57406012017-12-28 Interferon-α inhibits cell migration and invasion and induces the expression of antiviral proteins in Huh-7 cells transfected with hepatitis B virus X gene-expressing lentivirus Yang, Qian Li, Xiao-Peng Zhong, Yuan-Bin Xiang, Tian-Xin Zhang, Lun-Li Exp Ther Med Articles Hepatitis B virus (HBV) X protein (HBx) serves an important role in HBV infection and the development of HBV-related liver cancer. Interferon-α (IFN-α) is used to treat patients with HBV; however, the role of IFN-α in the development of HBV-related liver cancer remains unclear. The present study established a new HBV-related liver cancer model (Huh-7-HBx) by transfecting the hepatoma cell line Huh-7, with HBx-expressing lentivirus. Following IFN-α treatment, cell viability, migration and invasion, as well as the expression of antiviral proteins in Huh-7-HBx, were subsequently determined. The results demonstrated that HBx-expressing lentivirus had no significant effect on cell viability but promoted the migration and invasion of Huh-7 cells. The expression of the antiviral genes IFN α and β receptor subunit 1 (IFNAR1), IFNAR2, IFN-stimulated gene factor 3, double-stranded RNA-activated protein kinase and ribonuclease L, was also increased. Following treatment of Huh-7-HBx cells with IFN-α, the expression of antiviral genes was increased at the level of transcription and translation, whereas cell migration and invasion was decreased. The present study suggests that IFN-α may attenuate the development of HBV-related liver cancer by reducing cell migration and invasion and promoting the expression of antiviral proteins. D.A. Spandidos 2017-12 2017-10-11 /pmc/articles/PMC5740601/ /pubmed/29285141 http://dx.doi.org/10.3892/etm.2017.5288 Text en Copyright: © Yang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Yang, Qian Li, Xiao-Peng Zhong, Yuan-Bin Xiang, Tian-Xin Zhang, Lun-Li Interferon-α inhibits cell migration and invasion and induces the expression of antiviral proteins in Huh-7 cells transfected with hepatitis B virus X gene-expressing lentivirus |
title | Interferon-α inhibits cell migration and invasion and induces the expression of antiviral proteins in Huh-7 cells transfected with hepatitis B virus X gene-expressing lentivirus |
title_full | Interferon-α inhibits cell migration and invasion and induces the expression of antiviral proteins in Huh-7 cells transfected with hepatitis B virus X gene-expressing lentivirus |
title_fullStr | Interferon-α inhibits cell migration and invasion and induces the expression of antiviral proteins in Huh-7 cells transfected with hepatitis B virus X gene-expressing lentivirus |
title_full_unstemmed | Interferon-α inhibits cell migration and invasion and induces the expression of antiviral proteins in Huh-7 cells transfected with hepatitis B virus X gene-expressing lentivirus |
title_short | Interferon-α inhibits cell migration and invasion and induces the expression of antiviral proteins in Huh-7 cells transfected with hepatitis B virus X gene-expressing lentivirus |
title_sort | interferon-α inhibits cell migration and invasion and induces the expression of antiviral proteins in huh-7 cells transfected with hepatitis b virus x gene-expressing lentivirus |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5740601/ https://www.ncbi.nlm.nih.gov/pubmed/29285141 http://dx.doi.org/10.3892/etm.2017.5288 |
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