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. 2005;2(1):30-35.
doi: 10.7150/ijms.2.30. Epub 2005 Jan 5.

High level expression of apoptosis inhibitor in hepatoma cell line expressing Hepatitis B virus

Xuanyong Lu  1 , Matthew Lee, Trang Tran, Timothy Block
Affiliations

High level expression of apoptosis inhibitor in hepatoma cell line expressing Hepatitis B virus

Xuanyong Lu et al. Int J Med Sci. 2005.

Abstract

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.

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Conflict of interest statement

Conflict of interest: The authors have declared that no conflict of interest exists.

Figures

Figure 1
Figure 1
The over-expression of cIAP2 in the HBV expressing cell line, HepG2.215. The RNA from HepG2.215 and HepG2 cells were isolated. The expression of cIAP2 was examined with RT-PCR and Northern blot. A. RT-PCR detects cIAP2. One microgram RNA from HepG2 (number 1, duplicate) and HepG2.215 cells (number 2, duplicate) were reverse- transcripted, and then amplified by PCR. The result from PCR was shown as a 434bp band. β-Actin was used as a loading control. B. Northern blot detects cIAP2. Ten microgram RNA from HepG2 (number 1, duplicate) and HepG2.215 cells (number 2, duplicate) were separated by denature gel, then hybridized with cIAP2 specific probe. The cIAP2 and cIAP1 bands were indicated. β-Actin was used as a loading control as well.
Figure 2
Figure 2
The Detection of XIAP in the HepG2.215. The RNA from HepG2.215 and HepG2 cells were isolated. The expression of XIAP was examined with RT-PCR and Northern blot as described in Figure 1. A. RT-PCR detects XIAP. B. Northern blot detects XIAP. β-Actin was used as a loading control as well.
Figure 3
Figure 3
The up-regulation of cIAP2 protein in HepG2.215 cells. HepG2.215 cells were labeled by 35-S Met. The cIAP2 was immune-precipitated by anti-cIAP2 antibody, and then resolved in SDS PAGE. The images were analyzed by Phosphorimager.
See this image and copyright information in PMC

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