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首页> 外文期刊>Molecular and Cellular Biology >The v-fms oncogene induces factor-independent growth and transformation of the interleukin-3-dependent myeloid cell line FDC-P1.
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The v-fms oncogene induces factor-independent growth and transformation of the interleukin-3-dependent myeloid cell line FDC-P1.

机译：v-fms致癌基因诱导白细胞介素3依赖性骨髓细胞系FDC-P1的因子非依赖性生长和转化。

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The normal cellular counterpart of the v-fms oncogene product is a receptor for the mononuclear phagocyte colony-stimulating factor, CSF-1. An interleukin-3 (IL-3)-dependent mouse myeloid cell line, FDC-P1, was infected with a murine retrovirus vector containing v-fms linked to a gene encoding resistance to neomycin (neo). Infected cells selected for resistance to the aminoglycoside G418 contained few proviral DNA copies per haploid genome, expressed low levels of the v-fms-coded glycoprotein, remained IL-3 dependent for growth, and were nontumorigenic in nude mice. In contrast, infected cells selected for their ability to grow in the absence of IL-3 contained an increased number of proviral insertions, expressed high levels of the v-fms-coded glycoprotein, and were tumorigenic in nude mice. The IL-3-independent cells expressed IL-3 receptors of comparable number and affinity to those detected in uninfected FDC-P1 cells and did not produce a growth factor able to support replication of the parental cells. Thus, the synthesis of high levels of the v-fms gene product in FDC-P1 cells abrogated their requirement for IL-3 and rendered the cells tumorigenic by a nonautocrine mechanism. The data suggest that v-fms encodes a promiscuous tyrosine kinase able to transform cells of the myeloid lineage that do not normally express CSF-1 receptors.
机译：v-fms癌基因产物的正常细胞对应物是单核吞噬细胞集落刺激因子CSF-1的受体。白介素3（IL-3）依赖的小鼠骨髓细胞系FDC-P1被鼠逆转录病毒载体感染，该载体含有与编码新霉素抗性的基因相连的v-fms。被选为对氨基糖苷G418有抗性的感染细胞每个单倍体基因组几乎不含原病毒DNA拷贝，表达低水平的v-fms编码糖蛋白，仍然依赖IL-3的生长，并且在裸鼠中无致瘤性。相比之下，根据其在没有IL-3的情况下生长的能力而选择的感染细胞包含增加的前病毒插入数量，表达高水平的v-fms编码糖蛋白，并且在裸鼠中具有致瘤性。不依赖IL-3的细胞表达与未感染的FDC-P1细胞中检测到的IL-3受体具有相当数量和亲和力，并且不产生能够支持亲本细胞复制的生长因子。因此，在FDC-P1细胞中高水平的v-fms基因产物的合成废除了它们对IL-3的需求，并通过非自分泌机制使细胞致癌。数据表明，v-fms编码一种混杂的酪氨酸激酶，能够转化通常不表达CSF-1受体的髓系谱系的细胞。

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