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首页> 外文期刊>Molecular Carcinogenesis >Kinetics of myc-max-mad gene expression during hepatocyte proliferation in vivo: Differential regulation of mad family and stress-mediated induction of c-myc.
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Kinetics of myc-max-mad gene expression during hepatocyte proliferation in vivo: Differential regulation of mad family and stress-mediated induction of c-myc.

机译：体内肝细胞增殖过程中myc-max-mad基因表达的动力学：mad家族的差异调节和应激介导的c-myc诱导。

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摘要

Mad proteins (Mad1, Mxi1, Mad3, Mad4, Mnt/Rox) are biochemical and biological antagonists of c-Myc oncoprotein. Mad-Max dimers repress the transcription of the same target genes activated by Myc-Max dimers. Despite the critical role of Max and Mad proteins as modulators of c-Myc functions, there are no comparative data on their regulation in vivo. We carried out a systematic analysis of c-myc, max, and mad family expression in a model of synchronized cell proliferation in vivo in adult tissues, that is, rat hepatocytes after partial hepatectomy. We confirmed the previously reported early peak of c-myc expression after hepatectomy but we show that it did not correlate with hepatocyte proliferation as it also occurred in sham-operated animals as a result of surgical stresses. A second peak of c-myc expression was observed later, at the time of the wave of DNA synthesis. No such expression was detected in sham-operated rat quiescent hepatocytes. max expression increased around 4-16 h after hepatectomy, before the peaks of c-myc and DNA synthesis. mxi1 and mad4 were slightly downregulated during liver regeneration. mnt/rox expression did not change. These expression patterns suggest a role of Myc-Max for efficient mitogenic response of hepatocytes. We also analyzed the effects of Myc and Max ectopic expression on the clonogenic growth of the rat hepatoma cells. Expression of c-Myc and Max increased clonogenic growth, whereas the reduction of c-Myc levels by an antisense vector decreased growth. The results suggest nonredundant roles for mad genes in hepatocyte proliferation and point to c-Myc as a putative target for anticancer therapy of liver cancer.
机译：Mad蛋白（Mad1，Mxi1，Mad3，Mad4，Mnt / Rox）是c-Myc癌蛋白的生化和生物拮抗剂。 Mad-Max二聚体抑制Myc-Max二聚体激活的相同靶基因的转录。尽管Max和Mad蛋白作为c-Myc功能的调节剂发挥了关键作用，但尚无关于它们在体内调节的比较数据。我们在成年组织（即部分肝切除术后的大鼠肝细胞）体内同步细胞增殖模型中进行了c-myc，max和mad家族表达的系统分析。我们证实了先前报道的肝切除术后c-myc表达的早期峰值，但我们发现它与肝细胞增殖不相关，因为它在假手术动物中也由于手术压力而发生。后来在DNA合成浪潮时观察到了c-myc表达的第二个高峰。在假手术大鼠静止的肝细胞中未检测到这种表达。在肝切除术后4-16小时左右，在c-myc和DNA合成达到峰值之前，最大表达增加。在肝再生过程中，mxi1和mad4略有下调。 mnt / rox表达未改变。这些表达模式表明Myc-Max在肝细胞有效促有丝分裂反应中的作用。我们还分析了Myc和Max异位表达对大鼠肝癌细胞克隆生长的影响。 c-Myc和Max的表达增加了克隆形成的生长，而反义载体降低c-Myc的水平则减少了生长。结果表明，mad基因在肝细胞增殖中具有非冗余作用，并指出c-Myc是肝癌抗癌治疗的假定靶标。

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