The roles of reactive oxygen species (ROS) and autophagy in the survival and death of leukemia cells.
As a clonal disease of hematopoietic stem cells (HSCs), the etiology and pathogenesis of leukemia is not fully understood. Recent studies suggest that cellular homeostasis plays an essential role in maintaining the function of HSCs because dysregulation of cellular homeostasis is one of the major factors underlying the malignant transformation of HSCs. Reactive oxygen species (ROS) and autophagy, key factors regulating cellular homeostasis, are commonly observed in the human body. Autophagy can be induced by ROS through a variety of signaling pathways, and conversely inhibits ROS-induced damage to cells and tissues. ROS and autophagy coordinate to maintain cellular homeostasis. Previous studies have demonstrated that both of ROS and autophagy play important roles in the development of leukemia and are closely involved in drug resistance in leukemia. Interference with cellular homeostasis by promoting programmed leukemia cell death via ROS and autophagy has been verified to be an efficient technique in the treatment of leukemia. However, the critical roles of ROS and autophagy in the development of leukemia are largely unknown. In this review, we summarize the roles of ROS and autophagy in the pathogenesis of leukemia, which may allow the identification of novel targets and drugs for the treatment of leukemia based on the regulation of HSCs homeostasis through ROS and autophagy.
Department of Basic Medical Sciences, School of Medicine of Taizhou University, Taizhou 318000, Zhejiang, China; Institute of Tumor, School of Medicine of Taizhou University, Taizhou 318000, Zhejiang, China. Electronic address: cyfeng@tzc.edu.cn.
Yong-Feng
YF
Chen
School of Pharmacy, Shanghai Jiaotong University, Shanghai 200240, China.
Hao
H
Liu
Department of Basic Medical Sciences, School of Medicine of Taizhou University, Taizhou 318000, Zhejiang, China; Institute of Tumor, School of Medicine of Taizhou University, Taizhou 318000, Zhejiang, China.
Xin-Jing
XJ
Luo
Department of Basic Medical Sciences, School of Medicine of Taizhou University, Taizhou 318000, Zhejiang, China; Institute of Tumor, School of Medicine of Taizhou University, Taizhou 318000, Zhejiang, China.
Zhiqiang
Z
Zhao
Department of Basic Medical Sciences, School of Medicine of Taizhou University, Taizhou 318000, Zhejiang, China; Institute of Tumor, School of Medicine of Taizhou University, Taizhou 318000, Zhejiang, China; Biochemistry Department of Purdue University, West Lafayette, IN 47906, USA.
Zhen-You
ZY
Zou
Department of Histology and Embryology, North SiChuan Medical College, Nanchong 637000, Sichuan, China.
Jing
J
Li
Department of Hematology, the Affiliated Hospital of Guiyang Medical College, Guiyang 550004, China.
Xiao-Jing
XJ
Lin
Institute of Tumor, School of Medicine of Taizhou University, Taizhou 318000, Zhejiang, China. Electronic address: liangytzc@163.com.
Yong
Y
Liang
D001343:Autophagy / Q000502:physiology*; D006412:Hematopoietic Stem Cells / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007938:Leukemia / Q000378:metabolism / Q000473:pathology*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology
D017382:Reactive Oxygen Species
Autophagy; Drug resistance; Hematopoiesis; Homeostasis; Leukemia; Programmed cell death; Reactive oxygen species (ROS)