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人乳头状瘤病毒(HPV)感染和人子宫颈癌的发生密切相关,HPV致癌作用的主要基因为E6、E7。癌蛋白E6和E7通过与细胞抑癌基因p53和Rb蛋白产物作用并使之失活,导致细胞周期调节紊乱。近几年的一些研究结果表明,端粒酶是癌变过程诸多环节中关键一环,端粒酶活性可能成为临床检测宫颈癌一个重要的肿瘤标志物,E6、E7对端粒酶的表达调控也具有重要的影响。综述HPVE6、E7与端粒酶激活以及相互之间关系的相关机理研究。
Human papilloma virus (HPV) infection is closely related to the occurrence of human cervical cancer. The major genes responsible for HPV carcinogenesis are E6 and E7. Oncoproteins E6 and E7 cause cell cycle dysregulation by acting on and inactivating the cellular tumor suppressor genes p53 and Rb protein products. In recent years, some studies have shown that telomerase is a key link in many aspects of carcinogenesis. Telomerase activity may become an important tumor marker for clinical detection of cervical cancer. E6 and E7 regulate the expression of telomerase Has a significant impact. The mechanism of HPVE6, E7 and telomerase activation and their relationship with each other was reviewed.