Novel roles of reactive oxygen species in the pathogenesis of acute myeloid leukemia

被引:84
|
作者
Zhou, Fuling [1 ,5 ]
Shen, Qiang [2 ]
Claret, Francois X. [1 ,3 ,4 ]
机构
[1] Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Houston, TX 77030 USA
[2] Univ Texas MD Anderson Canc Ctr, Dept Clin Canc Prevent, Houston, TX 77030 USA
[3] Univ Texas Grad Sch Biomed Sci Houston, Expt Therapeut Acad Program, Houston, TX USA
[4] Univ Texas Grad Sch Biomed Sci Houston, Canc Biol Program, Houston, TX USA
[5] Xi An Jiao Tong Univ, Affiliated Hosp 2, Dept Clin Hematol, Xian, Shaanxi, Peoples R China
基金
中国国家自然科学基金;
关键词
ROS; cell signaling; leukemogenesis; MITOCHONDRIAL-DNA MUTATIONS; HEMATOPOIETIC STEM-CELLS; HISTAMINE DIHYDROCHLORIDE; TUMOR-SUPPRESSOR; HEME OXYGENASE-1; REDOX REGULATION; GENOMIC INSTABILITY; ROS PRODUCTION; SELF-RENEWAL; AML CELLS;
D O I
10.1189/jlb.0113006
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Review of ROS in the pathogenesis of acute myeloid leukemia (AML), and the rationale for redox therapies. 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.
引用
收藏
页码:423 / 429
页数:7
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