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首页> 外文期刊>Molecular and Cellular Biology >Coordinate regulation of myelomonocytic phenotype by v-myb and v-myc.
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Coordinate regulation of myelomonocytic phenotype by v-myb and v-myc.

机译：v-myb和v-myc协同调节粒细胞单核细胞表型。

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Both avian myeloblastosis virus (by the action of v-myb) and avian myelocytomatosis virus MC29 (by the action of v-myc) transform cells of the myelomonocytic lineage. Whereas avian myeloblastosis virus elicits a relatively immature phenotype, cells transformed by MC29 resemble mature macrophages. When cells previously transformed by v-myb were superinfected with MC29, their phenotype was rapidly altered to that of a more mature cell. These superinfected cells expressed both v-myb (at a level similar to that found before superinfection) and v-myc. It therefore appears that the expression of v-myc can elicit certain properties of a more differentiated phenotype. In addition, unlike cells transformed by v-myb alone, the cells expressing both v-myb and v-myc could not be induced by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate to differentiate to fully mature macrophages. Cells with a morphology similar to that of the superinfected cells were elicited by simultaneously infecting yolk sac macrophages with avian myeloblastosis virus and MC29. Such cells expressed both v-myb and v-myc. These results indicate that expression of v-myb and v-myc in infected cells coordinately regulates myelomonocytic phenotype and that the two viral oncogenes vary in their ability to interfere with tumor promoter-induced differentiation. Our findings also sustain previous suggestions that the oncogenes v-myb and v-myc may not transform target cells by simply blocking differentiation.
机译：禽骨髓成纤维细胞病病毒（通过v-myb的作用）和禽髓细胞增生病病毒MC29（通过v-myc的作用）都可以转化骨髓单核细胞系的细胞。禽成纤维细胞病病毒会引起相对不成熟的表型，而被MC29转化的细胞则类似于成熟的巨噬细胞。当先前由v-myb转化的细胞被MC29过度感染时，它们的表型迅速变为更成熟的细胞。这些超级感染的细胞同时表达v-myb（与超级感染前的水平相似）和v-myc。因此，似乎v-myc的表达可以引起更高分化的表型的某些特性。此外，与单独通过v-myb转化的细胞不同，表达v-myb和v-myc的细胞不能被肿瘤启动子12-O-十四烷酰phorbol-13-乙酸酯诱导分化为完全成熟的巨噬细胞。通过同时用禽成纤维细胞病病毒和MC29感染卵黄囊巨噬细胞来诱发形态与超感染细胞相似的细胞。这样的细胞表达v-myb和v-myc。这些结果表明受感染细胞中v-myb和v-myc的表达协调调节骨髓单核细胞表型，并且两种病毒癌基因在其干扰肿瘤启动子诱导的分化的能力方面有所不同。我们的发现还支持先前的建议，即癌基因v-myb和v-myc可能不会通过简单地阻止分化来转化靶细胞。

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