Bellon Marcia, Nicot Christophe
Department of Pathology and Laboratory Medicine, Center for Viral Oncology, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA.
Int J Cancer Oncol. 2015 Jun 2;2(2). doi: 10.15436/2377-0902.15.017.
While telomerase (hTERT) activity is absent from normal somatic cells, reactivation of hTERT expression is a hallmark of cancer cells. Telomerase activity is required for avoiding replicative senescence and supports immortalization of cellular proliferation. Only a minority of cancer cells rely on a telomerase-independent process known as alternative lengthening of telomeres, ALT, to sustain cancer cell proliferation. Multiple genetic, epigenetic, and viral mechanisms have been found to de-regulate telomerase gene expression, thereby increasing the risk of cellular transformation. Here, we review the different strategies used by the Human T-cell leukemia virus type 1, HTLV-I, to activate hTERT expression and stimulate its enzymatic activity in virally infected CD4 T cells. The implications of hTERT reactivation in HTLV-I pathogenesis and disease treatment are discussed.
虽然正常体细胞中不存在端粒酶（hTERT）活性，但hTERT表达的重新激活是癌细胞的一个标志。端粒酶活性是避免复制性衰老所必需的，并支持细胞增殖的永生化。只有少数癌细胞依赖一种称为端粒替代延长（ALT）的不依赖端粒酶的过程来维持癌细胞增殖。已发现多种遗传、表观遗传和病毒机制会失调端粒酶基因表达，从而增加细胞转化的风险。在这里，我们综述了1型人类T细胞白血病病毒（HTLV-I）在病毒感染的CD4 T细胞中激活hTERT表达并刺激其酶活性所使用的不同策略。还讨论了hTERT重新激活在HTLV-I发病机制和疾病治疗中的意义。
