Lang R A, Metcalf D, Gough N M, Dunn A R, Gonda T J
Cell. 1985 Dec;43(2 Pt 1):531-42. doi: 10.1016/0092-8674(85)90182-5.
Production of a growth factor by a cell that responds to this factor has been termed "autocrine" stimulation of proliferation. Considerable experimental data have suggested that tumor cells often exhibit autocrine growth stimulation and that this may contribute to the process of malignant transformation. To experimentally approach the relationship of autocrine growth stimulation to the malignant transformation of hemopoietic cells, we have used a retroviral vector to express sequences encoding a hemopoietic growth factor, granulocyte-macrophage colony stimulating factor (GM-CSF) in a factor-dependent murine cell line (FDC-P1). Virally infected cells synthesized and secreted GM-CSF, grew independently of exogenous CSF, and--unlike the parental FDC-P1 cells--produced tumors in syngeneic mice. We have thus experimentally induced autocrine growth regulation in a factor-dependent hemopoietic cell line and have shown that this results in tumorigenicity.
一个细胞产生能对该因子作出反应的生长因子,这一现象被称为增殖的“自分泌”刺激。大量实验数据表明,肿瘤细胞常常表现出自分泌生长刺激,这可能促成恶性转化过程。为了通过实验探究自分泌生长刺激与造血细胞恶性转化之间的关系,我们使用逆转录病毒载体在一个依赖因子的小鼠细胞系(FDC-P1)中表达编码造血生长因子粒细胞-巨噬细胞集落刺激因子(GM-CSF)的序列。病毒感染的细胞合成并分泌GM-CSF,不依赖外源性集落刺激因子生长,并且——与亲代FDC-P1细胞不同——在同基因小鼠中产生肿瘤。因此,我们通过实验在一个依赖因子的造血细胞系中诱导了自分泌生长调节,并表明这会导致致瘤性。