Pise-Masison Cynthia A, Brady John N
Virus Tumor Biology Section, Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 41 Room B201, 9000 Rockville Pike, Bethesda, MD 20892, USA.
Front Biosci. 2005 Jan 1;10:919-30. doi: 10.2741/1586.
Human T-lymphotropic virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia and tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). Although the precise mechanism of HTLV-1 oncogenesis remains unclear, the pathogenesis has been linked to the pleiotropic activity of the viral transcriptional activator protein Tax. Tax has been shown to regulate viral and cellular gene expression and to functionally interfere with proteins involved in cell-cycle progression and DNA repair. This review will concentrate on the ability of Tax to promote cellular proliferation through activation of the NF-kappaB pathway while inhibiting the cell-cycle checkpoint and apoptotic function of the tumor suppressor gene p53.
人类嗜T淋巴细胞病毒1型(HTLV-1)是成人T细胞白血病以及热带痉挛性截瘫/HTLV-1相关脊髓病(TSP/HAM)的病原体。尽管HTLV-1致癌的确切机制尚不清楚,但其发病机制与病毒转录激活蛋白Tax的多效性活动有关。Tax已被证明可调节病毒和细胞基因表达,并在功能上干扰参与细胞周期进程和DNA修复的蛋白质。本综述将集中探讨Tax通过激活NF-κB途径促进细胞增殖,同时抑制肿瘤抑制基因p53的细胞周期检查点和凋亡功能的能力。