ArticleInternational journal of cancer2010
Cooperation of tumor-derived HBx mutants and p53-249(ser) mutant in regulating cell proliferation, anchorage-independent growth and aneuploidy in a telomerase-immortalized normal human hepatocyte-derived cell line.
Article in International journal of cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Population attributable risk of aflatoxin-related liver cancer: systematic review and meta-analysis.European journal of cancer (Oxford, England : 1990) · 2012Pooled it
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- Aflatoxins and Human Health: Global Exposure, Disease Burden, and One Health Strategies.Toxins · 2026Review
- Associations of chronic liver disease and liver cancer with glyphosate and its metabolites in Thailand.International journal of cancer · 2025Article
- Integrative molecular characterisation of gallbladder cancer reveals micro-environment-associated subtypes.Journal of hepatology · 2021Article
- Genome-wide association study of the TP53 R249S mutation in hepatocellular carcinoma with aflatoxin B1 exposure and infection with hepatitis B virus.Journal of gastrointestinal oncology · 2020Article
- Prohibitin, STAT3 and SH2D4A physically and functionally interact in tumor cell mitochondria.Cell death & disease · 2020Article
- RNA Sequencing of Hepatobiliary Cancer Cell Lines: Data and Applications to Mutational and Transcriptomic Profiling.Cancers · 2020Article
- NOTCH target gene HES5 mediates oncogenic and tumor suppressive functions in hepatocarcinogenesis.Oncogene · 2020Article
- AGO2 MediatesMolecular cancer research : MCR · 2020Article
- Association of Aflatoxin and Gallbladder Cancer.Gastroenterology · 2017Article
- Oncogenic Activation of the RNA Binding Protein NELFE and MYC Signaling in Hepatocellular Carcinoma.Cancer cell · 2017Article
- Genetic alterations in hepatocellular carcinoma: An update.World journal of gastroenterology · 2016Review
- Somatic TP53 Mutations in the Era of Genome Sequencing.Cold Spring Harbor perspectives in medicine · 2016Review
- Negative reciprocal regulation between Sirt1 and Per2 modulates the circadian clock and aging.Scientific reports · 2016Article
- Transposon mouse models to elucidate the genetic mechanisms of hepatitis B viral induced hepatocellular carcinoma.World journal of gastroenterology · 2015Review
- Molecular mechanism of hepatitis B virus X protein function in hepatocarcinogenesis.World journal of gastroenterology · 2015Review
- Targeting Oncogenic Mutant p53 for Cancer Therapy.Frontiers in oncology · 2015Review
- Hepatitis B virus, HBx mutants and their role in hepatocellular carcinoma.World journal of gastroenterology · 2014Review
- Transcriptional regulation of the tumor suppressor FHL2 by p53 in human kidney and liver cells.PloS one · 2014Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
Abstract
Hepatocellular carcinoma (HCC) is a common cancer, and hepatitis B virus (HBV) is a major etiological agent. Convincing epidemiological and experimental evidence also links HCC to aflatoxin, a naturally occurring mycotoxin that produces a signature p53-249(ser) mutation. Recently, we have reported that tumor-derived HBx variants encoded by HBV exhibited attenuated transactivation and proapoptotic functions but retained their ability to block p53-mediated apoptosis. These results indicate that mutations in HBx may contribute to the development of HCC. In this study, we determined whether tumor-derived HBx mutants along, or in cooperation with p53-249(ser), could alter cell proliferation and chromosome stability of normal human hepatocytes. To test this hypothesis, we established a telomerase immortalized normal human hepatocycte line HHT4 that exhibited a near diploid karyotype and expressed many hepatocyte-specific genes. We found that overexpression one of the tumor-derived HBx mutants, CT, significantly increased colony forming efficiency (CFE) while its corresponding wild-type allele CNT significantly decreased CFE in HHT4 cells. p53-249(ser) rescued CNT-mediated inhibition of colony formation. Although HHT4 cells lacked an anchorage independent growth capability as they did not form any colonies in soft agar, the CT-expressing HHT4 cells could form colonies, which could be significantly enhanced by p53-249(ser). Induction of aneuploidy could be observed in HHT4 cells expressing CT, but additionally recurring chromosome abnormalities could only be detected in cells coexpressing CT and p53-249(ser). Our results are consistent with the hypothesis that certain mutations in HBx and p53 at codon 249 may cooperate in contributing to liver carcinogenesis.
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