Hines D L
Trudeau Institute, Saranac Lake, New York 12983.
Cancer Res. 1988 Apr 1;48(7):1702-7.
A cloned, virus-producing, tumorigenic, promonocytic leukemia cell line, AC8, derived from an Abelson murine leukemia virus-infected mouse can differentiate in vitro. Differentiated cells, purified from a population containing undifferentiated cells on the basis of expression of the macrophage differentiation antigens Mac-1 (C3 receptor) and F4/80, were phagocytic, produced lysozyme, were less tumorigenic, and had a reduced replicative capacity compared with undifferentiated cells. Differentiated cells produced less infectious Abelson virus than undifferentiation. Cloning studies indicated that differentiation was the cause rather than the effect of reduced Abelson virus production. However, the intracellular amount and the tyrosine-specific protein kinase activity of the Abelson virus oncogene product, P120v-abl, were not affected by differentiation of the leukemic cells. Thus, these results show that Abelson virus-transformed myeloid lineage cells can differentiate without expression of the viral oncogene product being affected, which implies, in turn, that P120v-abl expression is not sufficient for maintaining transformation by blocking differentiation.
一种克隆的、产生病毒的、致瘤性的原单核细胞白血病细胞系AC8,源自一只感染了阿贝尔森鼠白血病病毒的小鼠,它能够在体外分化。基于巨噬细胞分化抗原Mac-1(C3受体)和F4/80的表达,从含有未分化细胞的群体中纯化出的分化细胞具有吞噬作用、能产生溶菌酶、致瘤性较低,并且与未分化细胞相比,复制能力降低。分化细胞产生的感染性阿贝尔森病毒比未分化细胞少。克隆研究表明,分化是阿贝尔森病毒产生减少的原因而非结果。然而,白血病细胞的分化并未影响阿贝尔森病毒癌基因产物P120v-abl的细胞内含量和酪氨酸特异性蛋白激酶活性。因此,这些结果表明,阿贝尔森病毒转化的髓系细胞能够分化,而病毒癌基因产物的表达不受影响,这反过来意味着,P120v-abl的表达不足以通过阻断分化来维持转化状态。