Exp Mol Med.
2007 Aug;39(4):508-513.
Mutation analysis of p31(comet) gene, a negative regulator of Mad2, in human hepatocellular carcinoma
- Affiliations
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- 1Laboratory of Radiation Molecular OncologyDivision of Radiation Cancer Biology, Korea Institute of Radiological and Medical Sciences, Seoul 139-706, Korea. khlee@kcch.re.kr
- 2Department of Biochemistry, College of Medicine, Korea University, Seoul 136-701, Korea.
- 3Department of Biology, Department of Life and Nanopharmaceutical Sciences, Kyung Hee University, Seoul 130-701, Korea.
- 4National Cancer Center, Goyang 410-769, Korea.
- 5Laboratory of Toxicology, College of Verterinary Medicine, Nano Systems Institute-National Core Research Center, Seoul National University, Seoul 151-742, Korea.
Abstract
- Failure of mitotic checkpoint machinery leads to the chromosomal missegregation and nuclear endoreduplication, thereby driving the emergence of aneuploidy and tetraploidy population. Although abnormal nuclear ploidy and the resulting impairment of mitotic checkpoint function are typical physiological event leading to human hepatocellular carcinoma, any mutational change of mitotic checkpoint regulators has not yet been discovered. Therefore, we investigated the mutation of p31(comet), a recently identified mitotic checkpoint regulator, in human hepatocellular carcinoma. Of 51 human hepatocellular carcinoma tissue and 6 cell lines tested, five samples exhibited nucleotide sequence variations dispersed on four sites within the entire coding sequence. Among these sites with sequence substitutions, three were found to be missense mutation accompanied with amino acid change but one was a silent mutation. Of these sequence substitutions, two were present in both tumor and non-tumor liver tissues, suggesting the possibility of polymorphism. The present findings indicate that p31(comet) does not have an impact on the formation of aneuploidy and tetraploidy found in human hepatocellular carcinoma.
MeSH Terms
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Adaptor Proteins, Signal Transducing
Calcium-Binding Proteins/*metabolism
Carcinoma, Hepatocellular/genetics/*metabolism
Carrier Proteins/*genetics/metabolism
Cell Cycle Proteins/*genetics/*metabolism
Cell Line, Tumor
Humans
Liver Neoplasms/genetics/*metabolism
*Mutation
Nuclear Proteins
Polyploidy
Repressor Proteins/*metabolism
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