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Overexpression of cyclin D1 is an early event in, and possible mechanism responsible for, fumonisin B1 liver tumorigenesis in rats

  1. Author:
    Ramljak, D.
    Diwan, B. A.
    Ramakrishna, G.
    Victor, T. C.
    Marasas, W. F. O.
    Anderson, L. M.
    Gelderblom, W. C. A.
    1. Year of Conference: 1997
  2. Conference Name: Annual Meeting of the American Association for Cancer Research
    1. 38
    2. Pages: A3316
  4. Type of Work: Meeting Abstract
  1. Abstract:

    Fumonisin B1 (FB1), a mycotoxin produced by Fusarium moniliforme detected in 70% of U.S. corn-based food products, is hepatocarcinogenic in rats. Little is known about its carcinogenic mechanism; alteration in cell cycle progression has been suggested. We hypothesized that cyclin D1 might be overexpressed in response to FB1 and thus act as an oncogene. To investigate this we examined by immunohistochemistry eight paraffin-embedded hepatocellular carcinomas (HCC) caused by chronic FB1 feeding and five control livers, as well as HCC induced by chronic nitroglycerin or N-nitrosodiethylamine (1x; i.p.)/phenobarbital in diet. Cyclin D1 was indeed highly overexpressed in the tumors compared with normal liver, and only in HCC induced by FB1. In addition, we analyzed by immunoblot livers from animals fed 0, 50, 100 and 250 ppm of FB1 for 21 days, and found that cyclin D1 protein increased significantly in a dose-responsive manner, up to 20-fold, whereas no changes occurred in levels of cyclin dependent kinase (cdk4) or retinoblastoma protein (pRb), or in phosphorylation of pRb. It appears that cyclin D1 overexpression is an early event and possible mechanism responsible for FB1 carcinogenic effects.

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