人類乳突瘤病毒致癌轉機

HPV and cervical cancer related articles Part III- HPV carcinogenic mechanism

在子宮頸癌症組織與子宮頸癌細胞株中，我們經常可發現HPV的DNA插入宿主細胞染色體中。在這個穿插嵌入反應過程中，HPV的DNA須先由閉鎖的圓環型斷裂成為直線形，而斷裂點經常都固定發生在E1/E2序列，所以在斷裂處下游的E2、E4、E5、L1、L2等基因，經常被丟棄，不再繼續表現。無論這個穿插的過程是如何複雜與多變，病毒上游調控序列（URR），會伴隨E6與E7兩段基因一起，隨機嵌入宿主細胞染色體之非特定位置。眾所周知，單獨HPV感染並不足以導致子宮頸上皮細胞轉變成為癌症。HPV入侵後，還需要許多內在與外界協同因子共同的參與，導致宿主細胞內部發生複雜變化與多個基因先後發生突變，克服環境障礙與免疫監測，最終在部分患者演變成子宮頸癌症。 In cervical cancer tissue and cell lines, we often found that HPV DNA can insert into the host cell chromosome. During the insertion process, the circular HPV DNA must first be broken into a linear shape, and the breakpoints are always fixed in the E1/E2 sequence. Therefore, the E2, E4, E5, L1, L2, etc, are often discarded or no longer continue to express. No matter how complex the process would be, the viral upstream regulatory sequence (URR) and E6/E7 genes are randomly integrated into the host cell chromosomes. It is well known that the HPV infection alone is not enough to cause cervical cancer. However, HPV can cooperate with many intrinsic and extrinsic factors, which induce a series of complex intracellular reactions and gene mutations in host cells. After overcoming the host immune surveillance, cervical cancer develops in some cases.