【摘要】：宮頸癌是常見的女性惡性腫瘤,其發(fā)生發(fā)展與HPV的感染密切相關(guān)。HPV16是宮頸癌患者中感染率最高的亞型,其編碼的早期蛋白E5、E6、E7可刺激宮頸上皮細(xì)胞轉(zhuǎn)化成腫瘤細(xì)胞。E6、E7蛋白在宮頸癌晚期表達(dá),E5可能在早期表達(dá)。E5蛋白的是否表達(dá)及其致癌機(jī)制與多種因子相關(guān)。E5蛋白可作用于細(xì)胞生長因子受體通路,下調(diào)miRNA196a,并通過與HLAⅠ類分子結(jié)合協(xié)助感染細(xì)胞免疫逃逸,從而促進(jìn)腫瘤的發(fā)生。E5蛋白與E6、E7蛋白協(xié)同會(huì)發(fā)揮更強(qiáng)的致宮頸癌作用。本研究對(duì)E5蛋白表達(dá)與病毒整合的關(guān)系及其對(duì)宮頸癌的作用進(jìn)行了綜述。
[Abstract]:Cervical cancer is a common malignant tumor in women, and its occurrence and development are closely related to the infection of HPV. HPV16 is the subtype with the highest infection rate in patients with cervical cancer. Its early protein E5, E6, E7, can stimulate the transformation of cervical epithelial cells into tumor cells. E6 E7 protein is expressed in the late stage of cervical cancer, and E5 may be expressed in the early stage. The expression of E5 protein and its carcinogenic mechanism are related to many factors. For the cell growth factor receptor pathway, MiRNA196a, was down-regulated and the immune escape of infected cells was assisted by binding to HLA class 鈪，

本文編號(hào)：2265522