Foddis Rudy, De Rienzo Assunta, Broccoli Dominique, Bocchetta Maurizio, Stekala Elizabeth, Rizzo Paola, Tosolini Alessandra, Grobelny Jennifer V, Jhanwar Suresh C, Pass Harvey I, Testa Joseph R, Carbone Michele
Cancer Immunology Program, Department of Pathology, Cardinal Bernardin Cancer Center, Loyola University Chicago, Maywood, Illinois, IL 60153, USA.
Oncogene. 2002 Feb 21;21(9):1434-42. doi: 10.1038/sj.onc.1205203.
Mesotheliomas are malignant tumors of the pleural and peritoneal membranes which are often associated with asbestos exposure and with Simian virus 40 (SV40) infection. Telomerase activity is repressed in somatic cells and tissues but is activated in immortal and malignant cells. We evaluated telomerase activity in seven primary malignant mesothelioma biopsies and matched lung specimens and 20 mesothelioma cell lines and eight corresponding primary tumor cultures. All the tumor biopsies, and nearly all primary cell mesothelioma cultures and cell lines were telomerase positive. The findings in cell lines paralleled those observed in primary cultures in cases where paired samples were available. Next, we found that SV40, a DNA tumor virus present in approximately 50% of mesothelioma biopsies in the USA, induced telomerase activity in primary human mesothelial cells, but not in primary fibroblasts. Telomerase activity became detectable as early as 72 h following wild-type (strain 776) SV40 infection, and a clear DNA ladder was detectable 1 week after infection. The amount of telomerase activity increased during passage in cell culture and appeared to parallel increases in the cellular amounts of the SV40 large T-antigen. Thus, SV40 infection leads to telomerase activity before the infected mesothelial cells become transformed and immortalized. SV40 infection of human fibroblasts did not cause detectable telomerase activity. We also determined that the SV40 small t-antigen (tag) plays an important role in inducing telomerase activity because this activity was undetectable or minimal in mesothelial cells infected and/or transformed by SV40 tag mutants. Asbestos alone did not induce telomerase activity, and asbestos did not influence telomerase activity in mesothelial cells infected with SV40. Induction of telomerase activity by SV40 may be related to the very high rate of mesothelial cell immortalization that is characteristically associated with SV40 infection of mesothelial cells.
间皮瘤是胸膜和腹膜的恶性肿瘤,常与接触石棉以及感染猿猴病毒40(SV40)有关。端粒酶活性在体细胞和组织中受到抑制,但在永生化细胞和恶性细胞中被激活。我们评估了7例原发性恶性间皮瘤活检组织及配对的肺标本、20个间皮瘤细胞系和8个相应的原代肿瘤培养物中的端粒酶活性。所有肿瘤活检组织,以及几乎所有原代间皮瘤细胞培养物和细胞系的端粒酶均呈阳性。在有配对样本的情况下,细胞系中的结果与原代培养物中观察到的结果相似。接下来,我们发现,在美国约50%的间皮瘤活检组织中存在的DNA肿瘤病毒SV40,可诱导原代人胸膜间皮细胞产生端粒酶活性,但对原代成纤维细胞无此作用。野生型(776株)SV40感染后最早72小时即可检测到端粒酶活性,感染1周后可检测到明显的DNA梯带。在细胞培养传代过程中端粒酶活性量增加,且似乎与SV40大T抗原的细胞量增加平行。因此,在被感染的间皮细胞发生转化和永生化之前,SV40感染就导致了端粒酶活性。人成纤维细胞感染SV40未引起可检测到的端粒酶活性。我们还确定,SV40小t抗原(tag)在诱导端粒酶活性中起重要作用,因为在被SV40 tag突变体感染和/或转化的间皮细胞中,这种活性无法检测到或很低。单独的石棉不会诱导端粒酶活性,且石棉不影响感染SV40的间皮细胞中的端粒酶活性。SV40诱导端粒酶活性可能与间皮细胞永生化的高发生率有关,这是间皮细胞感染SV40的典型特征。