Anderson S M, Carroll P M, Lee F D
Department of Pathology, SUNY, Stony Brook 11794.
Oncogene. 1990 Mar;5(3):317-25.
We have investigated the ability of the v-src oncogene to abrogate growth factor dependent growth in the interleukin-3 dependent myeloid progenitor cell line 32D c13. Growth factor independent clones were isolated following infection of 32D c13 cells with murine retroviruses containing the v-src oncogene. v-src was demonstrated to be directly responsible for growth factor independence in experiments utilizing temperature-sensitive v-src mutants. The v-src infected cells released a growth factor capable of stimulating the proliferation of normal 32D c13 cells. Analysis of the mRNA from v-src infected 32D c13 did not identify the putative autocrine growth factor as one of the currently identified murine or human hematopoietic growth factors.
我们研究了v-src癌基因在白细胞介素-3依赖的髓系祖细胞系32D c13中消除生长因子依赖性生长的能力。在用含有v-src癌基因的鼠逆转录病毒感染32D c13细胞后，分离出了不依赖生长因子的克隆。在利用温度敏感型v-src突变体的实验中，v-src被证明是导致生长因子非依赖性的直接原因。v-src感染的细胞释放出一种能够刺激正常32D c13细胞增殖的生长因子。对v-src感染的32D c13细胞的mRNA分析并未将假定的自分泌生长因子鉴定为目前已鉴定的鼠或人造血生长因子之一。
