ArticleJournal of virology1996
Apoptosis is induced by N-myc expression in hepatocytes, a frequent event in hepadnavirus oncogenesis, and is blocked by insulin-like growth factor II.
Article in Journal of virology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 53 citations in OpenAlex.
- Application of the woodchuck animal model for the treatment of hepatitis B virus-induced liver cancer.World journal of gastrointestinal oncology · 2021Review
- ASK1 modulates the expression of microRNA Let7A in microglia under high glucose in vitro condition.Frontiers in cellular neuroscience · 2015Article
- N-myc augments death and attenuates protective effects of Bcl-2 in trophically stressed neuroblastoma cells.Oncogene · 2008Article
- Reactivation of the insulin-like growth factor-II signaling pathway in human hepatocellular carcinoma.World journal of gastroenterology · 2008Review
- Comparison of maturation, fertilization, development, and gene expression of mouse oocytes grown in vitro and in vivo.Journal of assisted reproduction and genetics · 2004Article
- Role of NF-kappaB and myc proteins in apoptosis induced by hepatitis B virus HBx protein.Journal of virology · 2001Article
- Article
- Hepatocellular carcinoma in WHV/N-myc2 transgenic mice: oncogenic mutations of beta-catenin and synergistic effect of p53 null alleles.Oncogene · 2000Article
- Hepatitis B virus biology.Microbiology and molecular biology reviews : MMBR · 2000Review
- Mechanisms of apoptosis by c-Myc.Oncogene · 1999Review
- 4E-BP1, a repressor of mRNA translation, is phosphorylated and inactivated by the Akt(PKB) signaling pathway.Genes & development · 1998Article
- Imprinted H19 oncofetal RNA is a candidate tumour marker for hepatocellular carcinoma.Molecular pathology : MP · 1998Article
- Selective expression of insulin-like growth factor II in the songbird brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1997Article
- Hepatitis B virus HBx protein sensitizes cells to apoptotic killing by tumor necrosis factor alpha.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Hepatitis B virus X antigen in the pathogenesis of chronic infections and the development of hepatocellular carcinoma.The American journal of pathology · 1997Review
- Insulin-like growth factor II blocks apoptosis of N-myc2-expressing woodchuck liver epithelial cells.Journal of virology · 1996Article
- Bcl-2 and M-Myc coexpression increases IGF-IR and features of malignant growth in neuroblastoma cell lines.Neoplasia (New York, N.Y.)Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Induction of hepatocellular carcinoma in woodchucks by woodchuck hepatitis virus is associated with the activation of N-myc gene expression, usually by viral DNA integration in cis to the N-myc locus. We have examined the consequences of N-myc up-regulation in rodent hepatic cells in culture. Mouse alpha ML hepatocytes infected with a retroviral vector overexpressing the woodchuck N-myc2 gene display a higher proliferation rate than parental alpha ML cells but are morphologically unchanged and do not form colonies in soft agar. However, they display an increased propensity to undergo apoptosis, an effect that is markedly augmented by serum deprivation. Expression of the woodchuck hepatitis virus X gene in alpha ML cells does not alter the growth phenotype of the cells and has no effect upon N-myc-dependent apoptosis. However, apoptosis in N-myc2-expressing alpha ML cells is strongly inhibited by insulin-like growth factor II (IGF II). IGF II gene expression is also strongly up-regulated during hepatic carcinogenesis in vivo in virally infected animals and has been speculated to be part of an autocrine growth-stimulatory pathway. Our results suggest that IGF II may play another role in the development of virus-induced hepatoma: the prevention of programmed cell death triggered by deregulated N-myc expression.
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