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Tumorigenesis in transgenic mice by a nuclear transport-defective SV40 large T-antigen gene

C A Pinkert, R L Brinster, R D Palmiter

    Virology
    |September 1, 1987
    PubMed

    Insights

    The Simian virus 40 (SV40) cT-ag mutant, defective in nuclear transport, causes brain tumors in transgenic mice. This highlights the oncogenic role of extranuclear SV40 large tumor antigen in vivo.

    Area of Science:

    • Oncology
    • Virology
    • Molecular Biology

    Background:

    • The Simian virus 40 (SV40) large tumor antigen (T-ag) is crucial for viral oncogenesis.
    • A specific mutant, SV40(cT), encodes a T-ag defective for nuclear transport.
    • This defect impacts its ability to transform cells and induce tumors in vivo.

    Purpose of the Study:

    • To investigate the in vivo biological activity of the transport-defective SV40 cT-ag.
    • To determine the oncogenic potential of cT-ag in a whole organism model.
    • To elucidate the role of extranuclear T-ag in tumor formation.

    Main Methods:

    • Generation of transgenic mice harboring the SV40(cT) gene.
    • Monitoring of tumor development and survival rates in transgenic mice.
    • Analysis of T-ag localization within tumor cells.

    Main Results:

    • Transgenic mice developed choroid plexus, renal, and thymic lesions.
    • A specific line of SV40(cT) transgenic mice consistently developed brain tumors.
    • SV40 T-ag was detected in the cytoplasm of tumor cells, not the nucleus.
    • SV40(cT) demonstrated oncogenic potential comparable to wild-type SV40 in this model.

    Conclusions:

    • Extranuclear SV40 T-ag plays a significant role in brain tumor formation.
    • In vitro cell transformation assays may not fully predict in vivo oncogenic potential.
    • The subcellular localization of T-ag is critical for its oncogenic mechanisms.

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