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单个v-Ki-ras基因的整合与缺失影响人骨肉瘤细胞的致瘤潜力。

Integration and loss of a single v-Ki-ras gene affects tumorigenic potential of human osteosarcoma cells.

作者信息

Carloni G, Venuat A M, Daya-Grosjean L, Nardeux P, Rhim J S, Azzarone B

机构信息

Istituto di Medicina Sperimentale, CNR, Rome, Italy.

出版信息

FEBS Lett. 1988 Mar 14;229(2):333-9. doi: 10.1016/0014-5793(88)81151-7.

DOI:10.1016/0014-5793(88)81151-7
PMID:2831097
Abstract

The human osteosarcoma cell line Te85 clone F-5 is not tumorigenic in vivo. Its transformation with Kirsten murine sarcoma virus (KiMSV) (KHOS) confers full malignant properties and stable non-tumorigenic revertants of this KHOS cell line have been obtained. Here we show that integration and expression of a single copy of the KiMSV proviral DNA, which is totally lost in the HOS 240S revertant, is responsible for the acquisition of tumorigenicity. Cytogenetic analysis and the absence of a residual LTR copy in the revertant cellular genome suggest that the loss of KiMSV provirus is caused either by chromosomal segregation or by recombination not involving the LTR. In addition analysis of the expression of ras proteins revealed no changes in the pattern of c-ras products and the expression of v-ras only in the KHOS cells. All these data suggest that Te85 and HOS 240S cell lines could represent a human alternative recipient system to rodent cells in studies with oncogenes.

摘要

人骨肉瘤细胞系Te85克隆F-5在体内不具有致瘤性。用柯斯顿鼠肉瘤病毒(KiMSV)对其进行转化(KHOS)可赋予其完全的恶性特性,并且已经获得了该KHOS细胞系稳定的非致瘤性回复突变体。在此我们表明,在HOS 240S回复突变体中完全缺失的单拷贝KiMSV前病毒DNA的整合和表达,是获得致瘤性的原因。细胞遗传学分析以及回复突变体细胞基因组中不存在残留的LTR拷贝表明,KiMSV前病毒的丢失是由染色体分离或不涉及LTR的重组引起的。此外,对ras蛋白表达的分析显示,c-ras产物的模式没有变化,而v-ras仅在KHOS细胞中表达。所有这些数据表明,在癌基因研究中,Te85和HOS 240S细胞系可代表一种替代啮齿动物细胞的人类受体系统。

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FEBS Lett. 1988 Mar 14;229(2):333-9. doi: 10.1016/0014-5793(88)81151-7.
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