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高危型人乳头瘤病毒(HR-HPV)感染是导致宫颈癌的重要原因。E5,E6,E7是HR-HPV编码的3种早期癌蛋白,对宫颈上皮细胞有刺激生长和转化功能。近期研究发现,E5在癌症发生的早期阶段通过干预生长因子受体,干扰细胞周期蛋白和细胞周期蛋白依赖激酶(CDKs),促进病毒癌基因的转化等过程发挥致癌作用。E6干预P53,使其对细胞生长负调节功能丧失,失去对细胞周期的正常调控,引起细胞无限增生并向恶性转化。E7干预视网膜母细胞瘤(Rb)蛋白,解除其抑制细胞增殖功能,发挥致癌作用。综述这3种早期癌蛋白致癌机制的研究进展。
High-risk human papillomavirus (HR-HPV) infection is an important cause of cervical cancer. E5, E6, E7 are three early oncoproteins encoded by HR-HPV, which stimulate the growth and transformation of cervical epithelial cells. Recent studies have found that E5 plays an oncogenic role in the early stages of cancer through interfering with growth factor receptors, interfering with cyclins and cyclin-dependent kinases (CDKs), and promoting the transformation of viral oncogenes. E6 intervention P53, its negative regulation of cell growth loss of function, loss of normal regulation of cell cycle, causing unlimited cell proliferation and malignant transformation. E7 intervention of retinoblastoma (Rb) protein, lifted its inhibition of cell proliferation function, play a carcinogenic effect. Review of these three kinds of early oncoprotein carcinogenesis research progress.