초록 열기/닫기 버튼
Failure of mitotic checkpoint machinery leads to the chromosomal missegregation and nuclear endore-duplication, thereby driving the emergence of aneu-ploidy 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 muta-tional change of mitotic checkpoint regulators has not yet been discovered. Therefore, we investigated the mutation of p31comet, a recently identified mitotic check-point regulator, in human hepatocellular carcinoma. Of 51 human hepatocellular carcinoma tissue and 6 cell lines tested, five samples exhibited nucleotide se-quence variations dispersed on four sites within the entire coding sequence. Among these sites with se-quence substitutions, three were found to be missense mutation accompanied with amino acid change but one was a silent mutation. Of these sequence sub-stitutions, two were present in both tumor and non-tu-mor liver tissues, suggesting the posibility of polymorphism. The present findings indicate that p31cometdoes not have an impact on the formation of aneuploidy and tetraploidy found in human hepatocel-lular carcinoma.
키워드열기/닫기 버튼
carcinoma, hepatocellular; MAD2L1 pro-tein, human; mitosis; mutation
