Bilello J A, Freedman V H, Shin S
J Natl Cancer Inst. 1977 Jun;58(6):1691-4. doi: 10.1093/jnci/58.6.1691.
Clonal isolates of the normal rat kidney cell line (NRK) transformed by a defective murine sarcoma virus (Kirsten strain) were injected into nude mice of BALB/c background to determine whether the growth of these cells as tumors was accompanied by the induction of host endogenous type C viruses. All the virus-transformed clones produced rapidly growing tumors in nude mice, but neither the induction of mouse endogenous viruses nor the rescue and spread of the transforming sarcoma virus were observed during the growth of tumors. The degree of expression of the tumor virus structural proteins in the transformed cells did not determine the cellular phenotype with regard to tumorigenicity in nude mice, nor did it modify the cellular growth properties in vitro. Consistent with earlier observations with simian virus 40-transformed mouse and rat cells, the ability of sarcoma virus-transformed NRK cells to initiate tumor growth in nude mice appeared to be correlated with anchorage-independent growth in vitro.
用缺陷型鼠肉瘤病毒(柯斯顿株)转化的正常大鼠肾细胞系(NRK)的克隆分离物被注射到BALB/c背景的裸鼠体内,以确定这些细胞作为肿瘤生长时是否伴随着宿主内源性C型病毒的诱导。所有病毒转化的克隆在裸鼠体内都产生了快速生长的肿瘤,但在肿瘤生长过程中,既未观察到小鼠内源性病毒的诱导,也未观察到转化肉瘤病毒的拯救和传播。转化细胞中肿瘤病毒结构蛋白的表达程度,既不能决定裸鼠体内肿瘤发生的细胞表型,也不能改变体外细胞的生长特性。与早期对猿猴病毒40转化的小鼠和大鼠细胞的观察结果一致,肉瘤病毒转化的NRK细胞在裸鼠体内启动肿瘤生长的能力似乎与体外不依赖贴壁生长相关。