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Activation of NF-κB by HTLV-I and implications for cell transformation

Abstract

T-cell transformation by the human T-cell leukemia virus type I (HTLV-I) involves deregulation of cellular transcription factors, including members of the NF-κB family. In normal T cells, NF-κB activation occurs transiently in response to immune stimuli, which is required for antigen-stimulated T-cell proliferation and survival. However, HTLV-I induces persistent activation of NF-κB, causing deregulated expression of a large array of cellular genes, which in turn contributes to the induction of T-cell transformation. The HTLV-I transforming protein Tax functions as an intracellular stimulator of IκB kinase (IKK), a cellular kinase mediating NF-κB activation by diverse stimuli. Tax physically interacts with IKK and renders this inducible kinase constitutively active. By assembling different Tax/IKK complexes, Tax targets the persistent activation of both canonical and noncanonical NF-κB signaling pathways. Whereas Tax plays a primary role in HTLV-I-mediated NF-κB activation, recent studies reveal that the IKK/NF-κB signaling pathway is also activated in freshly isolated adult T-cell leukemia (ATL) cells that often lack detectable Tax expression. The mechanism underlying this Tax-independent pathway of NF-κB activation remains poorly understood. Clarifying the precise nature and consequences of the constitutive NF-κB activation in ATL cells is important for developing rational therapeutic strategies for this T-cell malignancy.

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Acknowledgements

We thank members of the Sun and Yamaoka laboratories for critical reading of the manuscript. Research performed in the authors' laboratories on the subject under review was supported by research grants from the National Institutes of Health to S-CS (CA68471 and CA094922) and from the Ministry of Education, Culture, Sports, Science and Technology of Japan to SY (A119 and 17013029).

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Correspondence to Shao-Cong Sun or Shoji Yamaoka.

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Sun, SC., Yamaoka, S. Activation of NF-κB by HTLV-I and implications for cell transformation. Oncogene 24, 5952–5964 (2005). https://doi.org/10.1038/sj.onc.1208969

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