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首页> 外文期刊>Cell cycle >The AMPK-FoxO3A axis as a target for cancer treatment.
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The AMPK-FoxO3A axis as a target for cancer treatment.

机译：AMPK-FOXO3A轴作为癌症治疗的目标。

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摘要

FoxO proteins are an evolutionarily conserved subfamily of transcription factors involved in tumor suppression, regulation of energy metabolism and development in several tissues, and are mainly regulated by phosphorylation-dependent nuclear/cytoplasmic shuttling. The transcriptional activity of FoxO3A, one of the four members of the family, is further modulated by AMPK, one of the key regulators of cellular metabolism, which basically shifts cell machinery from energy-consuming to energy-producing pathways. We recently demonstrated that the AMPK/FoxO3A energy sensor pathway is still inducible in human cancer cells in response to metabolic stress, as it becomes activated in colorectal and ovarian cancer cells in response to the inhibition of p38alpha. Activation of the FoxO3A transcriptional program initially induces autophagy as an attempt to retain energy to survive, whereas under persistent stress conditions it triggers autophagic cell death. In this review, we focus on the connections between AMPK and FoxO3A, describing their central role as modulators of fundamental processes such as stress resistance, cell metabolism, autophagy and cell death, and highlighting the therapeutic potential of pharmacological modulation of the AMPK-FoxO3A axis.
机译：FOXO蛋白是一种参与肿瘤抑制的转录因子的进化遗传因子，在几种组织中调节能量代谢和发育，主要由磷酸化依赖性核/细胞梭上调节。 FoxO3A的转录活性是通过AMPK进一步调节细胞代谢的关键调节因子之一的AMPK进一步调节，基本上将细胞机械从能量消耗转移到能量产生的途径。我们最近证明了AMPK / Foxo3A能量传感器途径响应于代谢应激而诱导人类癌细胞，因为它在结肠直肠和卵巢癌细胞中被激活，响应于P38Alpha的抑制。 FoxO3A转录程序的激活最初诱导自噬作为试图保留能量以存活的尝试，而在持续的压力条件下，它触发了自噬细胞死亡。在这篇综述中，我们专注于AMPK和FOXO3A之间的连接，描述了它们作为基本过程的调节剂的中心作用，例如抗胁迫，细胞代谢，自噬和细胞死亡，并突出AMPK-FOXO3A轴的药理调节的治疗潜力。

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  • 来源
    《Cell cycle》 |2010年第6期|共6页
  • 作者

    Simone C;

  • 作者单位

    Laboratory of Signal-dependent Transcription Department of Translational Pharmacology (DTP);

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
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