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[致癌病毒SV40诱导的恶性转化的逆转。I. 接触抑制特性向正常类型的逆转诱导]

[Reversal of malignant transformation induced by the oncogenic virus SV40. I. Induction of reversal to normal type for the contact inhibition trait].

作者信息

Raevskaia G B, Varshaver N B, Gorbunova L V, Shapiro N I

出版信息

Genetika. 1987 Apr;23(4):662-9.

PMID:3034724
Abstract

The possibility of induction by the oncogenic DNA-containing virus SV40 of reversions to normal phenotype as regards contact inhibition ("flat" revertants), was studied in spontaneously transformed chinese hamster fibroblasts. Negative selection was used for detection of revertants. The method adopted allowed to study the mutagenic activity of the virus, while excluding its transforming effect. In all experiments the frequency of revertants after infection exceeded that in control series. The value of induction varied from 1.2 to 28.4 X 10(-6). The tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA) known to increase the frequency of mutations induced by carcinogens in vitro, displayed no enhancing effect on the frequency of revertants induced by SV40. The lack of enhancement of virus-induced reversions after TPA treatment might be explained by the lack of the transforming effect of SV40 in the system studied. Some of the normal "flat" colonies were T-antigen positive, i. e. the viral oncogene was expressed. The role of mutations induced by SV40 in cellular genes controlling malignancy is discussed.

摘要

在自发转化的中国仓鼠成纤维细胞中,研究了含致癌DNA的病毒SV40诱导细胞恢复正常表型(即接触抑制,“扁平”回复突变体)的可能性。采用阴性选择法来检测回复突变体。所采用的方法能够在排除病毒转化作用的同时,研究病毒的诱变活性。在所有实验中,感染后回复突变体的频率均超过了对照系列。诱导值在1.2至28.4×10⁻⁶之间变化。已知肿瘤促进剂12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯(TPA)可在体外增加致癌物诱导的突变频率,但对SV40诱导的回复突变体频率没有增强作用。TPA处理后病毒诱导的回复突变没有增强,这可能是由于在所研究的系统中SV40缺乏转化作用。一些正常的“扁平”集落T抗原呈阳性,即病毒癌基因得以表达。文中讨论了SV40诱导的细胞基因突变在控制恶性肿瘤的细胞基因中的作用。

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