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KMID : 0620920070390040508
Experimental & Molecular Medicine
2007 Volume.39 No. 4 p.508 ~ p.513
Mutation analysis of p31comet gene, a negative regulator of Mad2, in human hepatocellular carcinoma
Yun Mi-Yong

Kim Sang-Bum
Park Sun-Hoo
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
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 p31comet, 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 p31comet does not have an impact on the formation of aneuploidy and tetraploidy found in human hepatocellular carcinoma.
KEYWORD
carcinoma, hepatocellular, MAD2L1 protein, human, mitosis, mutation
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