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人乳头瘤病毒8型E7基因与激活的H-ras基因协同作用对原代大鼠胚胎成纤维细胞的致瘤转化

Tumorigenic transformation of primary rat embryonal fibroblasts by human papillomavirus type 8 E7 gene in collaboration with the activated H-ras gene.

作者信息

Nishikawa T, Yamashita T, Yamada T, Kobayashi H, Ohkawara A, Fujinaga K

机构信息

Department of Molecular Biology, Sapporo Medical College.

出版信息

Jpn J Cancer Res. 1991 Dec;82(12):1340-3. doi: 10.1111/j.1349-7006.1991.tb01802.x.

DOI:10.1111/j.1349-7006.1991.tb01802.x
PMID:1663918
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5918364/
Abstract

Particular types of human papillomavirus (HPV) are associated with skin cancer of epidermodysplasia verruciformis (EV) patients. Here, we show, for the first time, that the E7 gene of EV-associated HPV8 possesses a potential oncogenic transforming ability. The HPV8 E7 open reading frame (ORF) and the HPV16 E7 ORF were cloned under the SV40 promoter/enhancer to construct recombinant plasmids pcD2-8E7 and pcD2-16E7, respectively. Transfection of primary rat embryonal fibroblasts having an activated H-ras gene revealed that pcD2-8E7 as well as pcD2-16E7 induced transformation of cells in G418-resistant colonies at an efficiency of 12.3% and 42.9%, respectively. The resulting transformed cell lines induced by pcD2-8E7 and activated H-ras were tumorigenic when injected into syngeneic immunocompetent rats. The potential tumorigenicity of HPV8 E7 seemed to be higher than that of HPV16 E7.

摘要

特定类型的人乳头瘤病毒(HPV)与疣状表皮发育不良(EV)患者的皮肤癌有关。在此,我们首次表明,与EV相关的HPV8的E7基因具有潜在的致癌转化能力。将HPV8 E7开放阅读框(ORF)和HPV16 E7 ORF分别在SV40启动子/增强子下克隆,构建重组质粒pcD2 - 8E7和pcD2 - 16E7。对具有激活的H - ras基因的原代大鼠胚胎成纤维细胞进行转染后发现,pcD2 - 8E7以及pcD2 - 16E7分别以12.3%和42.9%的效率诱导细胞在G418抗性菌落中发生转化。由pcD2 - 8E7和激活的H - ras诱导产生的转化细胞系,注射到同基因免疫活性大鼠体内时具有致瘤性。HPV8 E7的潜在致瘤性似乎高于HPV16 E7。

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Tumorigenic transformation of primary rat embryonal fibroblasts by human papillomavirus type 8 E7 gene in collaboration with the activated H-ras gene.人乳头瘤病毒8型E7基因与激活的H-ras基因协同作用对原代大鼠胚胎成纤维细胞的致瘤转化
Jpn J Cancer Res. 1991 Dec;82(12):1340-3. doi: 10.1111/j.1349-7006.1991.tb01802.x.
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