Overexpression but Lack of Mutation and Methylation of p73 in Hepatocellular Carcinoma

Abstract

p73 is one of the family proteins that share structural and functional homologies with the tumor suppressor p53. To analyze the status of p73 in hepatocellular carcinoma (HCC), the allelic loss, allelic expression, mutation and methylation status of the p73 gene were examined in 18 paired HCC and normal tissues. No allelic loss was found. All heterozygous individuals contained RNA of both alleles, indicating that p73 was biallelically expressed in the liver. Notably, semiquantitative reverse transcriptase polymerase chain reaction analysis showed that p73 was consistently overexpressed in the cancerous tissues. Single-stranded conformation polymorphism and sequencing analysis revealed several polymorphisms, but no mutations were found in the entire coding sequence. Finally, the methylation patterns in the promoter and exon 1 regions of p73 were not altered in the cancerous tissues. These results do not support p73 as a tumor suppressor in HCC, but suggest that overexpression of p73 may in some way be associated with the pathogenesis of HCC.