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Heterozygous mice for the transforming growth factor-beta type II receptor gene have increased susceptibility to hepatocellular carcinogenesis

  1. Author:
    Im, Y. H.
    Kim, H. T.
    Kim, I. Y.
    Factor, V. M.
    Hahm, K. B.
    Anzano, M.
    Jang, J. J.
    Flanders, K.
    Haines, D. C.
    Thorgeirsson, S. S.
    Sizeland, A.
    Kim, S. J.

  2. Author Address

    NCI, Lab Cell Regulat & Carcinogensis, NIH, Bldg 41, Room B1106, Bethesda, MD 20892 USA. NCI, Lab Cell Regulat & Carcinogensis, NIH, Bethesda, MD 20892 USA. NCI, Expt Carcinogenesis Lab, Bethesda, MD 20892 USA. SAIC, Frederick Canc Res & Dev Ctr, Pathol Histotechnol Lab, Frederick, MD 21702 USA. Royal Melbourne Hosp, Ludwig Inst Canc Res, Melbourne, Vic 3050, Australia. Kim SJ NCI, Lab Cell Regulat & Carcinogensis, NIH, Bldg 41, Room B1106, Bethesda, MD 20892 USA.
    1. Year: 2001
  2. Journal: Cancer Research
    1. 61
    2. 18
    3. Pages: 6665-6668
  4. Type of Article: Article
  1. Abstract:

    The transforming growth factor-13 (TGF-13) receptor complex and its downstream signaling intermediates constitute a tumor suppressor pathway. In many cancers, expression of TGF-beta type 11 receptor (T betaR-II) is markedly decreased. In the present study, we show that the hepatocytes isolated from 15- day-old, but not 9-month-old, mice heterozygous for the deletion of the T betaR-II gene are slightly less sensitive to the growth-inhibitory effect of TGF-beta when compared with wild-type littermates of same age. In addition, the proliferation index of hepatocytes as indicated by bromodeoxyuridine incorporation is mildly increased in the heterozygous mice. These subtle changes in cellular phenotype did not result in either gross or microscopic abnormality of the liver. The treatment of these mice with the chemical carcinogen, diethyinitrosamine, results in a significantly enhanced tumorigenesis in the liver when compared with the wild-type littermates. Our results demonstrate the gene-dosage effect of T betaR-11 and indicate that the reduced expression of T betaR-11 in mice increases susceptibility to tumorigenesis in the liver.

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