人乳头瘤病毒E6/E7基因在宫颈癌发展过程中作用机制的研究  

Study on the mechanism of Human papillomavirus E6/E7 gene in the development of cervical cancer

作　　者：李明秀 刘志强[1] 许振[1] 杨世慧 LI Ming-xiu;LIU Zhi-qiang;XU Zhen;YANG Shi-hui(Department of Gynecology,Binzhou Medical University Hospital,Shandong Province,Binzhou 256600,China)

机构地区：[1]滨州医学院附属医院妇科,山东滨州256600

出　　处：《中国当代医药》2020年第16期23-26,30,共5页China Modern Medicine

摘　　要：目前,宫颈癌仍是全球范围内女性最常见的生殖系统恶性肿瘤,其中90%宫颈癌患者伴有人乳头瘤病毒(HPV)的感染,以高危型HPV 16和18型为主。高危型HPV E6/E7基因是造成细胞永生化和肿瘤进展的主要原因,病毒基因组整合到宿主基因组是癌基因E6和E7致癌的关键步骤,大量研究证实E6和E7基因可以导致p53和p Rb两个重要的抑癌基因失活,而最新的研究表明这两种基因可以作用于更多的细胞因子,如细胞的甲基化状态、PI3K-AKT通路、基质金属蛋白酶(MMPs)、白细胞介素-18(IL-18)等,对这些因子的不同影响最终导致了癌症的发生、转移及免疫逃逸等。At present,cervical cancer is still the most common reproductive system malignant tumor in women worldwide,and 90%of patients with cervical cancer are infected with Human papillomavirus(HPV),among which high-risk HPV types 16 and 18 are the main types.High-risk HPV E6/E7 gene is the main cause of cell immortalization and tumor progression.The integration of the viral genome into the host genome is a key step for oncogenes E6 and E7.A large number of studies have confirmed that E6 and E7 genes can lead to the inactivation of two important tumor suppressor genes,like p53 and pRb,the latest researches have shown these two genes can act on more cytokines,such as cell methylation status,PI3K AKT pathway,matrix metalloproteinases(MMPs),and interleukin-18(IL-18),and different effect on these factors ultimately lead to the occurrence,metastasis and immune escape of cancer.

关 键 词：E6/E7 人乳头瘤病毒 宫颈癌 PI3K-AKT 甲基化 基质金属蛋白酶 免疫机制 

分 类 号：R711[医药卫生—妇产科学]