Liver Cancer
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Feb 1, 2004; 10(3): 376-380
Published online Feb 1, 2004. doi: 10.3748/wjg.v10.i3.376
Hemizygous deletion and hypermethylation of RUNX3 gene in hepatocellular carcinoma
Wen-Hua Xiao, Wei-Wen Liu
Wen-Hua Xiao, Department of Oncology, 304th Hospital of PLA, Beijing 100037, China
Wei-Wen Liu, Department of Gastroenterology, Southwest Hospital, Third Military Medical University, Chongqing 400038, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Wen-Hua Xiao, PhD, Associate Professor, Department of Oncology, 304th Hospital of PLA, Beijing 100037, China.
Telephone: +86-10-66867324 Fax: +86-10-66867672
Received: May 11, 2003
Revised: May 25, 2003
Accepted: June 2, 2003
Published online: February 1, 2004

AIM: To analyze the genetic and epigenetic alterations of RUNX3 gene, a potential putative tumor suppressor gene, in hepatocellular carcinoma (HCC).

METHODS: PCR-based loss of heterozygosity (LOH) detection, analysis of mutation with PCR-single strand conformational polymorphism (SSCP) and sequencing, and methylation study with methylation specific PCR (MSP) were performed on RUNX3 gene in a series of 62 HCCs along with their matched normal tissues.

RESULTS: Mutation of RUNX3 gene was not found, but one single nucleotide polymorphism with T to A transversion at the second nucleotide of the 18th condon was found. Nine of 26 informative cases (34.6%) showed allelic loss on the polymorphic site and 30 cases (48.4%) revealed hypermethylation of RUNX3 gene in promoter CpG islands. Furthermore, of the 9 cases with LOH, 8 (88.9%) also had hypermethylation.

CONCLUSION: Our findings indicate that inactivation of RUNX3 gene through allelic loss and promoter hypermethylation might be one of the major mechanisms in hepatocellualr carcinogenesis.

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