國家衛生研究院 NHRI:Item 3990099045/4361
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    题名: Characterization of a glycine N-methyltransferase gene knockout mouse model for hepatocellular carcinoma: Implications of the gender disparity in liver cancer susceptibility
    作者: Liao, YJ;Liu, SP;Lee, CM;Yen, CH;Chuang, PC;Chen, CY;Tsai, TF;Huang, SF;Lee, YHW;Chen, YMA
    贡献者: Division of Molecular and Genomic Medicine
    摘要: Hepatocellular carcinoma (HCC) is the fifth common cancer in the world and it mainly occurs in men. Glycine N-methyltransferase (GNMT) participates in one-carbon metabolism and affects DNA methylation by regulating the ratio of S-adenosylmethionine to S-adenosylhomocystine. Previously, we described that the expression of GNMT was diminished in human HCC. Here, we showed that 50% (3/6) male and 100% (7/7) female Gnmt-/- mice developed HCC, and their mean ages of HCC development were 17 and 16.5 months, respectively. In addition, 42.9%, (3/7) of female Gnmt-/- mice had hemangioma. Writ reporter assay, demonstrated that Grunt is a negative regulator for canonical Writ signaling pathway. Beta-catenin, cyclin D1 and c-Myc, genes related to Wilt pathway, were upregulated in the liver tissues from both 11 weeks and HCC stage of Gnmt-/- mice. Furthermore, global DNA hypomethylation and aberrant expression of DNA methyltransferases 1 and 3b were found in the early and late stages of HCC development. Hierarchical cluster analysis of 6,023 transcripts from microarray data found that gene expression patterns of HCC tumors from male and female Gnmt-/- mice were distinctively different. Real-time PCR confirmed that Gadd45a, Pak1, Mapk3 and Dsup3 genes of mitogen-activated protein kinase (MAPK) pathway were activated in Gnmt-/- mice, especially in the female mice. Therefore, GNMT is a tumor suppressor gene for liver cancer, and it is associated with gender disparity in fiver cancer susceptibility.
    日期: 2009-02
    關聯: International Journal of Cancer. 2009 Feb;124(4):816-826.
    Link to: http://dx.doi.org/10.1002/ijc.23979
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0020-7136&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000262618400009
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=58149465911
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