p14ARF gene alterations in human hepatocellular carcinoma

Anzola, M.; Cuevas, N; López-Martı́nez, Mónica; Saiz, Alberto; Jj, Burgos; M, Martínez de Pancorboa

doi:10.1097/00042737-200401000-00004

Cited by 22 publications

(22 citation statements)

References 23 publications

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“…The presence of p14 methylation could be attributed to that P14 was reported to be preferentially methylated in HCV related HCC (Yang et al, 2003). Matching with our results, Anzola et al reported the methylation frequency of p14 in 41.9% out of 117 HCC cases (Anzola et al, 2004). Also, Liu et al (2006) reported the frequency of p14 methylation in 36% out of 50 HCC cases (Liu et al, 2006) but they did not include normal controls in their comparison as we did.…”

Section: Discussionsupporting

confidence: 90%

Disease Progression from Chronic Hepatitis C to Cirrhosis and Hepatocellular Carcinoma is Associated with Increasing DNA Promoter Methylation

Zekri

Nassar

Elrouby

et al. 2013

Asian Pacific Journal of Cancer Prevention

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The epigenetic changes observed in this study indicate that HCC tumors exhibit specific DNA methylation signatures with potential clinical applications in diagnosis and prognosis. In addition, methylation frequency could be used to monitor whether a patient with chronic hepatitis C is likely to progress to liver cirrhosis or even HCC. We can conclude that methylation processes are not just early events in hepatocarcinogenesis but accumulate with progression to cancer.

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Section: Discussionsupporting

confidence: 90%

Disease Progression from Chronic Hepatitis C to Cirrhosis and Hepatocellular Carcinoma is Associated with Increasing DNA Promoter Methylation

Zekri

Nassar

Elrouby

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…2 Recent advances in molecular genetics indicate that activation of oncogenes or inactivation of tumor suppressor genes might have an important role in HCC tumorigenesis. 3,4 Many studies demonstrated that abnormal changes in DNA methylation (including methylation content, level, and pattern) lead to the inactivation of some tumor suppressor genes, such as p16, p15, p14ARF, and RASSF, [5][6][7][8] which are involved in HCC carcinogenesis. These changes usually occur in 5'-CpG (5'-CG-3' palindrome; p, phosphate group) dinucleotides that are clustered frequently in regions approximately 1 to 2 kb long, called 5'-CpG islands, in or near the promoter and the first exon region of genes.…”

Section: Introductionmentioning

confidence: 99%

Promoter Hypermethylation of a Novel Gene,ZHX2,in Hepatocellular Carcinoma

Zhang

et al. 2006

Am J Clin Pathol

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We used methylation-sensitive restriction fingerprinting (MSRF) to identify novel CpG (5'-CG-3' palindrome; p, phosphate group)-rich sequences that are methylated differentially between the hepatocellular carcinoma (HCC) genomes and adjacent nontumorous liver tissues. A 199-base-pair sequence methylated in HCC tumor tissue was isolated and showed high homology to the 5' CpG island of the zinc fingers and homeoboxes protein 2 (ZHX2) gene. By using bisulfite sequencing, we confirmed that hypermethylation of the 5' CpG island of ZHX2 occurred in some HCC and HepG2 cell lines but not in 6 normal liver tissue samples. By using methylation-specific polymerase chain reaction, we detected methylation of the 5' CpG island of ZHX2 in 46.9% of the HCCs. Reverse transcription-polymerase chain reaction demonstrated that ZHX2 messenger RNA (mRNA) was expressed in all 6 normal liver tissue samples but in only 13.3% of the methylated HCCs. Treatment of HepG2 with 5-aza-deoxycytidine could demethylate the promoter and increase ZHX2 mRNA expression. These results suggest that hypermethylation-mediated silencing of ZHX2 is an epigenetic event involved in HCC.

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“…Although FoxM1 is over-expressed in HCC, the extent to which Arf is mutated or silenced in HCC is not clear. One study with 117 HCC samples provided evidence for loss of Arf expression by hypermethylation in about 42% of the samples and loss of heterozygosity in 27% of the samples (27). Also, it is possible that high-level expression of FoxM1 is able to overcome the Arf-regulation and induce development of aggressive HCC.…”

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confidence: 99%

FoxM1: A Master Regulator of Tumor Metastasis

2011

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The FoxM1 transcription factor gene is over-expressed in cancer. Its expression is stimulated by oncogenic signaling pathways and reactive oxygen species. It is also a target of regulation by the tumor suppressor genes. The transcriptional activity of FoxM1 depends upon activation by the Cyclin/Cdks as well as Plk1. FoxM1 stimulates expression of several genes involved in the cell cycle progression. Moreover, it supports proliferation of tumor cells by stimulating expression of the antioxidant genes and reducing oxidative stress. A new study provided evidence that FoxM1, in the absence of its inhibitor, the tumor suppressor Arf, drives metastasis of hepatocellular carcinoma (HCC). It induces an EMT-like phenotype in HCC cells, increases cell-migration and induces pre-metastatic niche at the distal organ of metastasis. FoxM1 directly activates genes involved in multiple steps of metastasis. In this review, we discuss the evidence for a master regulatory role of FoxM1 in tumor metastasis.

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p14ARF gene alterations in human hepatocellular carcinoma

Abstract: We can conclude that p14(ARF) is frequently and early altered in HCC, being the main cause of inactivation promoter hypermethylation. Our results suggest that the p14(ARF) gene plays an important role in the pathogenesis of hepatocellular carcinoma.

Cited by 22 publications

References 23 publications

Disease Progression from Chronic Hepatitis C to Cirrhosis and Hepatocellular Carcinoma is Associated with Increasing DNA Promoter Methylation

Disease Progression from Chronic Hepatitis C to Cirrhosis and Hepatocellular Carcinoma is Associated with Increasing DNA Promoter Methylation

Promoter Hypermethylation of a Novel Gene,ZHX2,in Hepatocellular Carcinoma

FoxM1: A Master Regulator of Tumor Metastasis

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