Lamsoul Isabelle, Lodewick Julie, Lebrun Sylvie, Brasseur Robert, Burny Arsène, Gaynor Richard B, Bex Françoise
Institute for Microbiological Research J-M Wiame, 1 Avenue E. Gryson, B-1070 Brussels, Belgium.
Mol Cell Biol. 2005 Dec;25(23):10391-406. doi: 10.1128/MCB.25.23.10391-10406.2005.
The transcription factor NF-kappaB is critical for the induction of cancer, including adult T-cell leukemia, which is linked to infection by human T-cell leukemia virus type 1 and the expression of its regulatory protein Tax. Although activation of the NF-kappaB pathway by Tax involves its interaction with the regulatory subunit of the IkappaB kinase (IKK) complex, NEMO/IKKgamma, the mechanism by which Tax activates specific cellular genes in the nucleus remains unknown. Here, we demonstrate that the attachment of SUMO-1 to Tax regulates its localization in nuclear bodies and the recruitment of both the RelA subunit of NF-kappaB and free IKKgamma in these nuclear structures. However, this sumoylation step is not sufficient for the activation of the NF-kappaB pathway by Tax. This activity requires the prior ubiquitination and colocalization of ubiquitinated Tax with IKK complexes in the cytoplasm and the subsequent migration of the RelA subunit of NF-kappaB to the nucleus. Thus, the ubiquitination and sumoylation of Tax function in concert to result in the migration of RelA to the nucleus and its accumulation with IKKgamma in nuclear bodies for activation of gene expression. These modifications may result in targets for the treatment of adult T-cell leukemia.
转录因子核因子-κB(NF-κB)对于癌症的诱导至关重要,包括成人T细胞白血病,该病与人T细胞白血病病毒1型感染及其调节蛋白Tax的表达有关。尽管Tax对NF-κB途径的激活涉及其与IκB激酶(IKK)复合物的调节亚基NEMO/IKKγ的相互作用,但Tax在细胞核中激活特定细胞基因的机制仍不清楚。在此,我们证明SUMO-1与Tax的结合调节其在核体中的定位以及NF-κB的RelA亚基和游离IKKγ在这些核结构中的募集。然而,这一SUMO化步骤不足以使Tax激活NF-κB途径。该活性需要Tax先进行泛素化并在细胞质中与IKK复合物共定位,随后NF-κB的RelA亚基迁移至细胞核。因此,Tax的泛素化和SUMO化协同作用,导致RelA迁移至细胞核并与IKKγ在核体中积累,从而激活基因表达。这些修饰可能成为成人T细胞白血病治疗的靶点。