Hepatitis B virus-induced oncogenesis

Lupberger, Joachim

doi:10.3748/wjg.v13.i1.74

Cited by 238 publications

(196 citation statements)

References 106 publications

Supporting

Mentioning

191

Contrasting

Unclassified

Order By: Relevance

“…HBV infection can promote carcinogenesis by at least 3 different mechanisms (27)(28)(29). First, insertional mutations of HBV are known to activate endogenous genes with involvement in cell cycle control, cellular proliferation, and differentiation.…”

Section: Of ---------------------------------------mentioning

confidence: 99%

Expression and role of SIRT1 in hepatocellular carcinoma

Choi

Bae²,

Jamiyandorj³

et al. 2011

Oncol Rep

View full text Add to dashboard Cite

Abstract. silent mating type information regulation 2 homolog 1 (sIrt1) is a multifaceted, nicotinamide adenine dinucleotide-dependent protein deacetylase with involvement in a wide variety of cellular processes ranging from cancer to aging. expression of sIrt1 was evaluated in 90 cases of hepatocellular carcinoma (HCC) and five HCC cell lines. The relationship between the mutation status of p53 and expression of sIrt1 was also investigated in 10 fresh HCC tissues. synthetic small interfering rNA was used to silence sIrt1 gene expression by rNA interference (rNAi), and cell growth and cell cycle progression were assessed. expression of sIrt1 was significantly elevated in the HCC tissues when compared to that of non-tumor tissues (p<0.001). Overexpression of sIrt1 and p53 was observed in 56% (50 of 90) and in 30% (27 of 90) of the HCCs, respectively. expression of sIrt1 showed significant correlation with gender (p=0.023), serum AFP levels (p=0.030), viral infection (p=0.005) and p53 expression (p<0.021). Western blot analysis found no correlation between p53 mutation and expression levels of sIrt1. sIrt1 silencing was found to induce cell growth arrest in HCC cells. these results suggest an association of sIrt1 expression with HCC development and that sIrt1 plays a role in cancer cell growth.

show abstract

Section: Of ---------------------------------------mentioning

confidence: 99%

Expression and role of SIRT1 in hepatocellular carcinoma

Choi

Bae²,

Jamiyandorj³

et al. 2011

Oncol Rep

View full text Add to dashboard Cite

show abstract

“…HBV codes for several proteins from four known genes (P, S, X and C). The P gene codes for DNA polymerase; the S gene for three polypeptides (HBs) of different sizes (large, medium and small); X for an HBx protein that is thought to be involved in hepatocarcinogenesis; and C for the core protein (Seeger and Mason, 2000;zur Hausen, 2006;Beck and Nassal, 2007;Lupberger and Hildt, 2007).…”

Section: Hepatitis B Virusmentioning

confidence: 99%

“…HBx protein and various HBs envelope proteins seem to be responsible for the alteration of major signaling pathways, including the NF-kB and Wnt/b-catenin pathways, which deregulate normal cell processes (Lupberger and Hildt, 2007;Gurtsevitch, 2008). HBV infection is also thought to generate genomic instability through viral DNA integration or through the activity of viral proteins, producing loss and gain of chromosomal DNA, allelic losses (loss of heterozygosity, LOH), transpositions and mutations of key genes such as p53, RB or hTERT (Horikawa and Barrett, 2003;Cougot et al, 2005;Lupberger and Hildt, 2007;Gurtsevitch, 2008).…”

Section: Hepatitis B Virusmentioning

confidence: 99%

“…HBV infection is also thought to generate genomic instability through viral DNA integration or through the activity of viral proteins, producing loss and gain of chromosomal DNA, allelic losses (loss of heterozygosity, LOH), transpositions and mutations of key genes such as p53, RB or hTERT (Horikawa and Barrett, 2003;Cougot et al, 2005;Lupberger and Hildt, 2007;Gurtsevitch, 2008).…”

Section: Hepatitis B Virusmentioning

confidence: 99%

See 1 more Smart Citation

Viral epigenomes in human tumorigenesis

Fernández

Esteller

2010

Oncogene

View full text Add to dashboard Cite

Viruses are associated with 15-20% of human cancers worldwide. In the last century, many studies were directed towards elucidating the molecular mechanisms and genetic alterations by which viruses cause cancer. The importance of epigenetics in the regulation of gene expression has prompted the investigation of virus and host interactions not only at the genetic level but also at the epigenetic level. In this study, we summarize the published epigenetic information relating to the genomes of viruses directly or indirectly associated with the establishment of tumorigenic processes. We also review aspects such as viral replication and latency associated with epigenetic changes and summarize what is known about epigenetic alterations in host genomes and the implications of these for the tumoral process. The advances made in characterizing epigenetic features in cancer-causing viruses have improved our understanding of their functional mechanisms. Knowledge of the epigenetic changes that occur in the genome of these viruses should provide us with markers for following cancer progression, as well as new tools for cancer therapy.

show abstract

“…The mechanism by which HBV promotes oncogenesis is still unclear. A viral nonstructural gene product (X protein) may be involved; alternatively or additionally, virus-induced chronic inflammation and repair as a result of immune-mediated hepatocyte necrosis may promote cellular transformation [23].…”

Section: Hepatitis B Virus (Hbv)mentioning

confidence: 99%