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Tumor Biology

Increased Expression of the Insulin-like Growth Factor I (IGF-I) Receptor Gene in Hepatocellular Carcinoma Cell Lines: Implications of IGF-I Receptor Gene Activation by Hepatitis B Virus X Gene Product

Sun-Ok Kim, Jae-Gahb Park and Young Ik Lee
Sun-Ok Kim
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Jae-Gahb Park
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Young Ik Lee
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DOI:  Published August 1996
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Abstract

Hepatitis B virus infection is associated with acute and chronic liver disease and the development of hepatocellular carcinoma (hcc). Several lines of evidence have suggested that hepatitis B virus X protein (HBx), which is a transcriptional trans-activator, plays a role in the process of liver carcinogenesis. We have investigated the expression of insulin-like growth factor I (IGF-I) receptor in human hepatocellular carcinoma cell lines using SNU368 cells containing HBx and SNU387 cells, which lack HBx gene transcript (J-G. Park et al., Int. J. Cancer, 62: 276–282, 1995), in an attempt to understand its possible relationship to the HBx-induced hcc. The binding of 125I-labeled IGF-I to the SNU368 cells was 5-fold higher than that of SNU387 cells. The Scatchard analysis of the binding data revealed a single class binding site for IGF-I with Kd of 7.6 and 8.8 nm and maximum binding capacities of 169 and 33 fmol/105 cells, respectively. Therefore, the difference observed in 125I-labeled IGF-I binding between SNU368 and SNU387 cells was due to an increase in the number of IGF-I binding sites with no change in affinity for the IGF-I receptor. An enhanced level of IGF-I receptors in SNU368 cells was also observed by fluorescence-activated cell sorting analysis using a monoclonal antibody against human IGF-I receptor, αIR3. The level of IGF-I receptor RNA and the basal IGF-I receptor gene promoter activity in SNU368 cells were 5 and 10 times higher than those observed in SNU387 cells, respectively. To substantiate further that HBx could transactivate the expression of the endogenous IGF-I receptor gene, Hep G2 cells were transiently transfected with a HBx expression vector. The transfection of Hep G2 cells with an HBx expression vector resulted in increased levels of IGF-I receptor RNA, promoter activity, and 125I-labeled IGF-I binding by 2.6-, 2.8-, and 2-fold, respectively. As a result of higher levels of IGF-I receptor, the mitogenic effect of IGFs (IGF-I and IGF-II) on SNU368 cells was 6 times higher than that of SNU387 cells. These results suggest that HBx may play a role in the process of hcc by activating IGF-I receptor gene expression.

Footnotes

  • ↵1 This work was supported by a grant from Korea Ministry of Science and Technology (G71131M).

  • ↵2 To whom requests for reprints should be addressed.

  • Received February 16, 1996.
  • Accepted June 18, 1996.
  • ©1996 American Association for Cancer Research.
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August 1996
Volume 56, Issue 16
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Increased Expression of the Insulin-like Growth Factor I (IGF-I) Receptor Gene in Hepatocellular Carcinoma Cell Lines: Implications of IGF-I Receptor Gene Activation by Hepatitis B Virus X Gene Product
Sun-Ok Kim, Jae-Gahb Park and Young Ik Lee
Cancer Res August 15 1996 (56) (16) 3831-3836;

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Increased Expression of the Insulin-like Growth Factor I (IGF-I) Receptor Gene in Hepatocellular Carcinoma Cell Lines: Implications of IGF-I Receptor Gene Activation by Hepatitis B Virus X Gene Product
Sun-Ok Kim, Jae-Gahb Park and Young Ik Lee
Cancer Res August 15 1996 (56) (16) 3831-3836;
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