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High level expression of apoptosis inhibitor in hepatoma cell line expressing Hepatitis B virus
The serious result of hepatitis B (HBV) virus infection is development of hepatocellular carcinoma (HCC). However, the reason of development of HCC in HBV infected patients is still unclear. Recently, the suppression of cell apoptosis is found to relate with the development of cell carcinogenesis, t...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
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Ivyspring International Publisher
2005
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1142222/ https://www.ncbi.nlm.nih.gov/pubmed/15968337 |
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author | Lu, Xuanyong Lee, Matthew Tran, Trang Block, Timothy |
author_facet | Lu, Xuanyong Lee, Matthew Tran, Trang Block, Timothy |
author_sort | Lu, Xuanyong |
collection | PubMed |
description | The serious result of hepatitis B (HBV) virus infection is development of hepatocellular carcinoma (HCC). However, the reason of development of HCC in HBV infected patients is still unclear. Recently, the suppression of cell apoptosis is found to relate with the development of cell carcinogenesis, therefore, the expression of apoptosis inhibitor in the virus related cancer line such as hepatoma cell line HepG2.215 was investigated. There are at least six Human apoptosis inhibitors (IAP) have been identified now. They are cIAP1, cIAP2, XIAP, NAPI, survivin and pIAP. Using gene-assay technology, we have recently compared the expression of IAPs in the HepG2.215 cells that persistently expresses Hepatitis B virus by integrated HBV genome with its parent cell line HepG2. The results suggest that there was obviously increase of cIAP2 and cIAP1 in the HepG2.215 cells versus HepG2 cells. Those observations imply a possibility of long time HBV infection could induce the over-expressing apoptosis inhibitors, furthermore, causing the liver cancer. The high expression of cIAP1 and cIAP2 in HBV expressing cells was confirmed by RT-PCR and Northern blot analysis. However, we did not find the change of NIAP and suvivin in HepG2.215 cells. In contrast, the expression of XIAP was down in the HepG2.215 cells comparing with HepG2 cells. How HBV triggers the over-expression of apoptosis inhibitor is unclear. Transient transfection of HepG2 cells with the plasmids expressing different HBV proteins such as S, M, L, X and core proteins did not give a decisive conclusion. Further study is going on now. |
format | Text |
id | pubmed-1142222 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2005 |
publisher | Ivyspring International Publisher |
record_format | MEDLINE/PubMed |
spelling | pubmed-11422222005-06-17 High level expression of apoptosis inhibitor in hepatoma cell line expressing Hepatitis B virus Lu, Xuanyong Lee, Matthew Tran, Trang Block, Timothy Int J Med Sci Research Paper The serious result of hepatitis B (HBV) virus infection is development of hepatocellular carcinoma (HCC). However, the reason of development of HCC in HBV infected patients is still unclear. Recently, the suppression of cell apoptosis is found to relate with the development of cell carcinogenesis, therefore, the expression of apoptosis inhibitor in the virus related cancer line such as hepatoma cell line HepG2.215 was investigated. There are at least six Human apoptosis inhibitors (IAP) have been identified now. They are cIAP1, cIAP2, XIAP, NAPI, survivin and pIAP. Using gene-assay technology, we have recently compared the expression of IAPs in the HepG2.215 cells that persistently expresses Hepatitis B virus by integrated HBV genome with its parent cell line HepG2. The results suggest that there was obviously increase of cIAP2 and cIAP1 in the HepG2.215 cells versus HepG2 cells. Those observations imply a possibility of long time HBV infection could induce the over-expressing apoptosis inhibitors, furthermore, causing the liver cancer. The high expression of cIAP1 and cIAP2 in HBV expressing cells was confirmed by RT-PCR and Northern blot analysis. However, we did not find the change of NIAP and suvivin in HepG2.215 cells. In contrast, the expression of XIAP was down in the HepG2.215 cells comparing with HepG2 cells. How HBV triggers the over-expression of apoptosis inhibitor is unclear. Transient transfection of HepG2 cells with the plasmids expressing different HBV proteins such as S, M, L, X and core proteins did not give a decisive conclusion. Further study is going on now. Ivyspring International Publisher 2005-01-05 /pmc/articles/PMC1142222/ /pubmed/15968337 Text en © Ivyspring International Publisher. This is an open access article distributed under the terms of a Creative Commons License (http://creativecommons.org/licenses/by-nc-nd/2.0) which permits distribution and reproduction for noncommerical purposes, provided that the article is in whole, unmodified, and properly cited. |
spellingShingle | Research Paper Lu, Xuanyong Lee, Matthew Tran, Trang Block, Timothy High level expression of apoptosis inhibitor in hepatoma cell line expressing Hepatitis B virus |
title | High level expression of apoptosis inhibitor in hepatoma cell line expressing Hepatitis B virus |
title_full | High level expression of apoptosis inhibitor in hepatoma cell line expressing Hepatitis B virus |
title_fullStr | High level expression of apoptosis inhibitor in hepatoma cell line expressing Hepatitis B virus |
title_full_unstemmed | High level expression of apoptosis inhibitor in hepatoma cell line expressing Hepatitis B virus |
title_short | High level expression of apoptosis inhibitor in hepatoma cell line expressing Hepatitis B virus |
title_sort | high level expression of apoptosis inhibitor in hepatoma cell line expressing hepatitis b virus |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1142222/ https://www.ncbi.nlm.nih.gov/pubmed/15968337 |
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