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Use of Mouse JB6 Cells to Identify Molecular Targets and Novel Agents for Prevention of Carcinogenesis

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Food Factors for Cancer Prevention

Summary

Identification of the natural or synthetic agents that block the rate-limiting phase of tumor promotion is essential to the goal of cancer prevention. In vitro model systems to study the promotion process and to screen potential preventive agents continue to be important. One well established system representing preneoplastic to neoplastic progression is the JB6 murine epidermal model, which consists of promotion-resistant (P-) and promotion-sensitive (P+) preneoplastic cell lines as well as irreversibly transformed, tumorigenic cell lines. The model has been used to study the molecular mechanisms of tumor promotion, identify potential promoters and promotion inhibitors, elucidate differences between neoplastic and preneoplastic cells (e.g., identification of genes required for maintenance of tumor phenotype), and evaluate agents for reversion potential. Additionally, apoptosis response variants of one of the tumorigenic JB6 lines allow the study of programmed cell death, a process important to the prevention of or susceptibility to carcinogenesis. Exogenous promoters such as the phorbol esters and endogenous promoters such as epidermal growth factor, transforming growth factor, and tumor necrosis factor induce the anchorage-independent transformation of P+ cells. The antipromoting activity of a number of agents having cancer prevention potential has been demonstrated using P+ cells. These agents include classic antipromoters such as retinoic acid and food factors such as green or black tea and curcumin. Important insights into the mechanism of neoplastic transformation have been gained from comparison of JB6 P+ and P- cells, most notably the requirement for induction of transcription factor AP-1 transactivation activity. This understanding has led to the development of small molecule and transgene agents aimed at specifically blocking AP-1 activity; they are under evaluation for their ability to block cancer development.

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Authors and Affiliations

  1. Gene Regulation Section, Laboratory of Biochemical Physiology, Frederick Cancer Research and Development Center, National Cancer Institute, Building 560, Room 21-4, Frederick, MD, 21702, USA

    Joan L. Cmarik & Nancy H. Colburn

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  1. Joan L. Cmarik
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  2. Nancy H. Colburn
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Editors and Affiliations

  1. Department of Food Science and Technology Faculty of Agriculture, Kyoto University, Oiwake-cho, Kitashirakawa, Kakyo-ku, Kyoto, 606-01, Japan

    Hajime Ohigashi Ph.D. (Professor) (Professor)

  2. Department of Applied Biological Sciences Faculty of Agriculture, Nagoya University, Furocho, Chikusa-ku, Nagoya, Aichi, 464-01, Japan

    Toshihiko Osawa Ph.D. (Professor) (Professor)

  3. Lipid Science Laboratory, National Food Research Institute, Ministry of Agriculture, Forestry and Fisheries, 2-1-2 Kannondai, Tsukuba, Ibaraki 305, Japan

    Junji Terao Ph.D. (Head) (Head)

  4. Nutrition and Epidemiology, Department of Agriculture, Tokyo University of Agriculture, 1-1-1 Sakuragaoka, Setagaya-ku, Tokyo 156, Japan

    Shaw Watanabe M.D. (Professor) (Professor)

  5. First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602, Japan

    Toshikazu Yoshikawa M.D. (Associate Professor) (Associate Professor)

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Cmarik, J.L., Colburn, N.H. (1997). Use of Mouse JB6 Cells to Identify Molecular Targets and Novel Agents for Prevention of Carcinogenesis. In: Ohigashi, H., Osawa, T., Terao, J., Watanabe, S., Yoshikawa, T. (eds) Food Factors for Cancer Prevention. Springer, Tokyo. https://doi.org/10.1007/978-4-431-67017-9_13

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  • DOI: https://doi.org/10.1007/978-4-431-67017-9_13

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