Mutation analysis of p31(comet) gene, a negative regulator of Mad2, in human hepatocellular carcinoma.
- Author:
Mi Yong YUN
1
;
Sang Bum KIM
;
Sunhoo PARK
;
Chul Ju HAN
;
Young Hoon HAN
;
Sun Hee YOON
;
Sang Hoon KIM
;
Chang Min KIM
;
Dong Wook CHOI
;
Myung Haing CHO
;
Gil Hong PARK
;
Kee Ho LEE
Author Information
1. Laboratory of Radiation Molecular OncologyDivision of Radiation Cancer Biology, Korea Institute of Radiological and Medical Sciences, Seoul 139-706, Korea. khlee@kcch.re.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
carcinoma, hepatocellular;
MAD2L1 protein, human;
mitosis;
mutation
- MeSH:
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
- From:Experimental & Molecular Medicine
2007;39(4):508-513
- CountryRepublic of Korea
- Language:English
-
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.
