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对一些源自人类的皮肤和生殖器乳头瘤病毒的E6和E7基因转化3Y1细胞能力的比较研究。

Comparative study on E6 and E7 genes of some cutaneous and genital papillomaviruses of human origin for their ability to transform 3Y1 cells.

作者信息

Hiraiwa A, Kiyono T, Segawa K, Utsumi K R, Ohashi M, Ishibashi M

机构信息

Laboratory of Viral Oncology, Aichi Cancer Center, Nagoya, Japan.

出版信息

Virology. 1993 Jan;192(1):102-11. doi: 10.1006/viro.1993.1012.

DOI:10.1006/viro.1993.1012
PMID:8390746
Abstract

E6 (or E7) genes of some genital and cutaneous human papillomaviruses (HPVs) were compared for their ability to transform cells of a rat fibroblastic line (3Y1) by using recombinant retroviruses. The E6 gene of genital cancer-associated HPV 16 or 18 was found to induce a characteristic morphological change, i.e., densely packed arrays of elongated cells forming swirl patterns. This change is the same as that induced by the E6 gene of cutaneous cancer-associated HPV 5, 8, or 47, which we described previously. The E6 gene of HPV 1 or 11, associated with benign tumor of cutaneous or genital tissue, respectively, induced no such change. The E6 genes of all these cutaneous and genital HPVs enhanced anchorage-independent growth of the target cells induced by E7 gene of HPV 16 or 18, and this enhancing activity of HPVs 16, 18, and 47 was stronger than that of HPVs 1 and 11. A distinct type of morphological transformation of 3Y1 cells, i.e., rounded miniaturized cells that were densely packed without forming any distinctive arrays, was found to be induced strongly by E7 genes of HPVs 16 and 18, weakly by E7 of HPVs 1 and 11, and not at all by E7 of HPV 47. The results suggest that the intensity of the morphological change induced by E6 genes, rather than E7 genes, is correlated to the risk of malignant conversion of the lesion with which the corresponding HPVs are associated.

摘要

通过使用重组逆转录病毒,比较了一些生殖器和皮肤型人乳头瘤病毒(HPV)的E6(或E7)基因转化大鼠成纤维细胞系(3Y1)细胞的能力。发现与生殖器癌相关的HPV 16或18的E6基因可诱导一种特征性的形态变化,即形成漩涡状图案的细长细胞紧密排列。这种变化与我们之前描述的与皮肤癌相关的HPV 5、8或47的E6基因所诱导的变化相同。分别与皮肤或生殖器组织良性肿瘤相关的HPV 1或11的E6基因未诱导出这种变化。所有这些皮肤和生殖器HPV的E6基因均增强了由HPV 16或18的E7基因诱导的靶细胞的非锚定依赖性生长,并且HPV 16、18和47的这种增强活性强于HPV 1和11。发现3Y1细胞的一种独特类型的形态转化,即紧密堆积而不形成任何独特排列的圆形小型化细胞,由HPV 16和18的E7基因强烈诱导,由HPV 1和11的E7基因弱诱导,而HPV 47的E7基因则完全不诱导。结果表明,由E6基因而非E7基因诱导的形态变化强度与相应HPV相关病变的恶性转化风险相关。

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