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Molecular mechanisms of cellular transformation by HTLV-1 Tax

Oncogene volume 24, pages 5976–5985 (2005)Cite this article

Abstract

The HTLV Tax protein is crucial for viral replication and for initiating malignant transformation leading to the development of adult T-cell leukemia. Tax has been shown to be oncogenic, since it transforms and immortalizes rodent fibroblasts and human T-lymphocytes. Through CREB, NF-κB and SRF pathways Tax transactivates cellular promoters including those of cytokines (IL-13, IL-15), cytokine receptors (IL-2Rα) and costimulatory surface receptors (OX40/OX40L) leading to upregulated protein expression and activated signaling cascades (e.g. Jak/STAT, PI3Kinase, JNK). Tax also stimulates cell growth by direct binding to cyclin-dependent kinase holenzymes and/or inactivating tumor suppressors (e.g. p53, DLG). Moreover, Tax silences cellular checkpoints, which guard against DNA structural damage and chromosomal missegregation, thereby favoring the manifestation of a mutator phenotype in cells.

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Acknowledgements

This work was supported in part by DFG (Grant SFB466-TPC3) and Wilhelm Sander-Stiftung (to RG). We thank Anthony Elmo for assistance with manuscript preparation.

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  1. Institut für Klinische und Molekulare Virologie, Universität Erlangen-Nürnberg, Schlossgarten 4, Germany

    Ralph Grassmann

  2. Department of Microbiology, Ben-Gurion University, Beer Sheva, Israel

    Mordechai Aboud

  3. Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, MD, USA

    Kuan-Teh Jeang

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Grassmann, R., Aboud, M. & Jeang, KT. Molecular mechanisms of cellular transformation by HTLV-1 Tax. Oncogene 24, 5976–5985 (2005). https://doi.org/10.1038/sj.onc.1208978

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