Activation of the IGF-II Gene by HBV-X Protein Requires PKC and p44/p42 Map Kinase Signalings

Kang-Park, Suk Mi; Lee, Je Ho; Shin, Jeh Hoon; Lee, Young Ik

doi:10.1006/bbrc.2001.4767

Cited by 38 publications

(25 citation statements)

References 24 publications

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“…The HBV-derived HBx protein in particular has been shown to increase IGF-II expression, presumably owing to SP1-mediated reactivation of fetal-type IGF-II promoters Kang-Park et al, 2001). The HCV-derived core gene product also acts as a transactivator and therefore induces expression of IGF-II from P4 through SP1 and EGR-1 binding sites .…”

Section: Signaling Pathways and Their Dysregulationmentioning

confidence: 99%

Dysregulation of growth factor signaling in human hepatocellular carcinoma

2006

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Section: Signaling Pathways and Their Dysregulationmentioning

confidence: 99%

Dysregulation of growth factor signaling in human hepatocellular carcinoma

2006

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“…24,27,37 Genes involved in cell growth regulation located at the Hcrem2 locus include Adra2a and Adrb1, encoding adrenergic receptors ␣2a and ␤1, respectively, and Prkg1 and Cyp17, which are deregulated in rat and/or human HCC. 38,39 Cyp17 encodes cytochrome P-450-17␣, which mediates 17␣-hydroxylase and 17,20-lyase activities in the androgen biosynthesis pathway. It is a susceptibility gene for prostate cancer in men 40 and interacts with steroid 5␣-reductase type II and androgen receptor genes, resulting in increased risk of HCC in humans.…”

Section: Epistatic Locimentioning

confidence: 99%

Phenotypic reversion of rat neoplastic liver nodules is under genetic control

Miglio

Simile

Muroni

et al. 2003

Intl Journal of Cancer

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Low DNA synthesis and high redifferentiation (remodeling) characterize neoplastic nodules induced by chemical carcinogens in hybrid BFF1 rats, generated by crossing the susceptible F344 and resistant BN strains. We performed whole-genome scanning of BFF2 rats to identify loci controlling remodeling of nodules induced, 32 weeks after initiation with diethylnitrosamine, by the RH protocol. Remodeling nodules were identified as areas lacking uniformity of GST-P immunostaining and with irregular margins. Two loci in suggestive linkage with the percentage of remodeling nodules were identified on chromosomes 7 and 1 (LOD scores 3.85 and 2.9 at D7Rat25 and D1Mgh14). Significant dosage-negative effect of the B allele on remodeling and additive interaction between these loci were found. Individual risk of liver cancer reflects the amount of exposure to environmental agents, such as hepatitis B and hepatitis C viruses, aflatoxin B1, ethanol consumption, etc., combined with one's genetic predisposition. [1][2][3][4] Owing to the difficulty of studying the genetic mechanisms of human liver cancer, interspecies comparison has been proposed to identify susceptibility and resistance alleles responsible for polygenic control of the predisposition to human HCC. Previous studies on a murine model of hepatocarcinogenesis have led to the identification of 7 hepatocarcinogenesis susceptibility loci (Hcs1-7) and 2 resistance loci (Hcr1 and Hcr2) in crosses between susceptible and resistant strains. 5-8 Moreover, 2 susceptibility loci (hepatocarcinogenesis in female, Hcf1 and Hcf2) abrogate the inhibitory effect of ovarian hormones on liver tumorigenesis in mice. 9 Study of the genetic control of rat HCC in the hybrid strain BFF1, generated in our laboratory by crossing the BN, resistant, to the F344, susceptible, strains, 10 has shown dominant inheritance of resistance to hepatocarcinogenesis. Linkage analysis of BFF1 ϫ F344 backcross and BFF2 intercross rats 11,12 revealed the presence of 4 Hcs loci (rat Hcs1-4) and 7 Hcr loci (rat Hcr1-7). Hcs3 and Hcr2 have also been identified, and named Dhr1 and Drh2, in intercrosses between the (F344 ϫ DRH)F1 rats. 13 A putative suppressor gene (rccϩ), mapping to chromosome 12p, critical for determining the sensitivity of rats to diethylnitrosamine-induced liver carcinogenesis, has been identified in MHC-recombinant rat ACP strains, congenic for the MHC-linked growth reproduction complex (grc) region. 14 Clonal expansion of initiated cells in rat liver carcinogenesis is characterized by the progressive development of foci of preneoplastic hepatocytes and neoplastic nodules exhibiting fast growth and a number of morphologic, biochemical and molecular commonalties with preneoplastic and neoplastic human liver lesions. 4,15,16 Most early preneoplastic and neoplastic liver lesions undergo progressive decreases in biochemical marker expression and growth rate and finally regress (remodeling, phenotypic reversion [17][18][19][20][21][22] ). Relatively few persistent lesions are thought to be precurso...

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“…HBx activates MAP kinase by increasing GTP uptake onto Ras [12,13]. Unlike growth factor activation of Ras, HBx increases Ras signaling moderately and over a prolonged period of time [11].…”

mentioning

confidence: 99%