Department of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
J Leukoc Biol. 2013 Sep;94(3):423-9. doi: 10.1189/jlb.0113006. Epub 2013 May 28.
It has become apparent that regulation of ROS is important in cell signaling and homeostasis. Accumulation of ROS triggers oxidative stress in various cell types and contributes to the development, progression, and persistence of cancer. Recent research has demonstrated that redox dysregulation caused by ROS promotes proliferation, differentiation, genomic, and epigenetic alterations; immune evasion; and survival in leukemic cells. ROS act as signaling molecules to regulate redox-sensitive transcriptional factors, enzymes, oncogenes, and other downstream effectors. Thus, a thorough understanding the role of ROS as key mediators in leukemogenesis is likely to provide opportunities for improved pharmacological intervention. In this review, we summarize the recent findings that support a role for ROS in the pathogenesis of AML and outline innovative approaches in the implementation of redox therapies for myeloid malignancies.
已经很明显，ROS 的调节在细胞信号转导和内稳态中很重要。ROS 的积累会在各种细胞类型中引发氧化应激，并导致癌症的发展、进展和持续存在。最近的研究表明，ROS 引起的氧化还原失调促进了白血病细胞的增殖、分化、基因组和表观遗传改变、免疫逃逸和存活。ROS 作为信号分子调节氧化还原敏感的转录因子、酶、癌基因和其他下游效应物。因此，深入了解 ROS 作为白血病发生的关键介质的作用可能为改善药理学干预提供机会。在这篇综述中，我们总结了支持 ROS 在 AML 发病机制中作用的最新发现，并概述了用于髓系恶性肿瘤的氧化还原治疗的创新方法。
