C - myc和Max在蛋白激酶C修饰剂诱导的K562细胞巨核细胞和单核巨噬细胞分化中的调控作用:C - myc下调但不抑制分化。

A Lerga, P Crespo, M Berciano, M D Delgado, M Cañelles, C Calés, C Richard, E Ceballos, P Gutierrez, N Ajenjo, S Gutkind, J León
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引用次数: 0

摘要

我们研究了C - myc和Max在蛋白激酶C (PKC)激活剂和抑制剂12- o -十四烷醇-13醋酸酯(TPA)和staurosporine诱导的K562细胞分化途径中的调控和作用。我们通过细胞超微结构、血小板形成和DNA内复制发现,星孢素诱导巨核细胞分化。相反,TPA诱导的分化表型更接近于单核-巨噬细胞谱系。在TPA和staurosporine分化的K562中,c-myc的表达均下调,而max的表达在两种情况下均未改变。虽然PKC酶活性在TPA和staurosporine终末分化的细胞中较低,但PKC活性本身的抑制并不会诱导c-myc下调。我们得出结论,由于这些药物以独立于PKC的方式触发分化过程,c-myc基因被关闭。K562细胞中c-Myc的异位过表达不影响单核-巨噬细胞和巨核细胞的分化,这表明在K562中这些过程不需要c-Myc的抑制。同样,两种分化途径都不受Max过表达或c-Myc和Max同时过表达的影响。这一结果与c-Myc对K562红系分化的抑制作用形成对比,提示c-Myc/Max在不同分化途径中发挥不同的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Regulation of c-Myc and Max in megakaryocytic and monocytic-macrophagic differentiation of K562 cells induced by protein kinase C modifiers: c-Myc is down-regulated but does not inhibit differentiation.

We have studied the regulation and role of c-Myc and Max in the differentiation pathways induced in K562 cells by 12-O-tetradecanoyl phorbol-13 acetate (TPA) and staurosporine, an activator and inhibitor, respectively, of protein kinase C (PKC). We found that staurosporine induced megakaryocytic differentiation, as revealed by the cellular ultrastructure, platelet formation, and DNA endoreduplication. In contrast, TPA induced a differentiated phenotype that more closely resembled that of the monocyte-macrophage lineage. c-myc expression was down-regulated in K562 differentiated by both TPA and staurosporine, whereas max expression did not change in either case. Although PKC enzymatic activity was low in cells terminally differentiated with TPA and staurosporine, inhibition of PKC activity by itself did not induce c-myc down-regulation. We conclude that the c-myc gene is switched off as a consequence of the differentiation process triggered by these drugs in a manner independent from PKC. Ectopic overexpression of c-Myc in K562 cells did not affect the monocytic-macrophagic and megakaryocytic differentiation, indicating that c-Myc suppression is not required for these processes in K562. Similarly, both differentiation pathways were not affected by Max overexpression or by concomitant overexpression of c-Myc and Max. This result is in contrast with the inhibition of erythroid differentiation of K562 exerted by c-Myc, suggesting divergent roles for c-Myc/Max, depending on the differentiation pathway.

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