论文部分内容阅读
人乳头状瘤病毒(HPV)是双链闭环小分子DNA病毒,基因组全长约8kb,组成6个早期表达基因(E6、E7、E1、E2、E4、E5)和2个晚期表达基因(L1、L2)。高危型HPV的E6和E7基因是病毒癌基因。E6和E7蛋白分别结合和降解P53和PRb蛋白,导致细胞周期失控、染色体不稳定、基因扩增、丢失和突变等改变,从而促使宫颈肿瘤的发生和发展。HPV导致宫颈肿瘤的病理机制包括持续性感染、E6和E7基因表达和蛋白功能的改变、HPV整合至宿主细胞DNA等,其中以E6和E7基因表达和蛋白功能的改变为中心。E6和E7蛋白的功能状态决定宫颈上皮内肿瘤的进退和浸润癌的恶性形状的维持和演进,但具体机制还不清楚。进一步研究与E6和E7蛋白相互作用的分子及其机理将可揭示宫颈肿瘤发生发展的病理规律,为最终控制宫颈癌打下基础。
Human papillomavirus (HPV) is a double-stranded, closed-loop, small-molecule DNA virus with a total length of about 8kb and consists of 6 early expressed genes (E6, E7, E1, E2, E4, E5) and 2 late expressed genes , L2). The high-risk HPV E6 and E7 genes are viral oncogenes. E6 and E7 proteins, respectively, combine and degrade P53 and PRb proteins, resulting in uncontrolled cell cycle, chromosomal instability, gene amplification, loss and mutation, which in turn promote the occurrence and development of cervical cancer. Pathological mechanism of HPV-induced cervical cancer include persistent infection, E6 and E7 gene expression and protein function changes, HPV integration into the host cell DNA and so on, in which E6 and E7 gene expression and protein function changes as the center. The functional status of E6 and E7 proteins determines the maintenance and progression of cervical intraepithelial neoplasia and malignant shape of invasive carcinoma, but the exact mechanism is unclear. Further study of the interaction between E6 and E7 protein molecules and their mechanisms will reveal the development of cervical tumor pathology, lay the foundation for the ultimate control of cervical cancer.