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Mutation analysis of p31comet gene, a negative regulator of Mad2, in human hepatocellular carcinoma
Authors:Yun Mi-Yong  Kim Sang Bum  Park Sunhoo  Han Chul Ju  Han Young-Hoon  Yoon Sun Hee  Kim Sang Hoon  Kim Chang-Min  Choi Dong-Wook  Cho Myung-Haing  Park Gil-Hong  Lee Kee-Ho
Institution:Laboratory of Radiation Molecular Oncology, Division of Radiation Cancer Biology, Korea Institute of Radiological and Medical Sciences, Department of Biochemistry, College of Medicine, Korea University, Seoul 136-701, 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.
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