Redox Control in Acute Lymphoblastic Leukemia: From Physiology to Pathology and Therapeutic Opportunities

Acute lymphoblastic leukemia (ALL) is a hematological malignancy originating from B- or T-lymphoid progenitor cells. Recent studies have shown that redox dysregulation caused by overproduction of reactive oxygen species (ROS) has an important role in the development and progression of leukemia. The...

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Main Authors: Yongfeng Chen, Jing Li, Zhiqiang Zhao
Format: Article
Language:English
Published: MDPI AG 2021-05-01
Series:Cells
Subjects:
Online Access:https://www.mdpi.com/2073-4409/10/5/1218
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author Yongfeng Chen
Jing Li
Zhiqiang Zhao
author_facet Yongfeng Chen
Jing Li
Zhiqiang Zhao
author_sort Yongfeng Chen
collection DOAJ
description Acute lymphoblastic leukemia (ALL) is a hematological malignancy originating from B- or T-lymphoid progenitor cells. Recent studies have shown that redox dysregulation caused by overproduction of reactive oxygen species (ROS) has an important role in the development and progression of leukemia. The application of pro-oxidant therapy, which targets redox dysregulation, has achieved satisfactory results in alleviating the conditions of and improving the survival rate for patients with ALL. However, drug resistance and side effects are two major challenges that must be addressed in pro-oxidant therapy. Oxidative stress can activate a variety of antioxidant mechanisms to help leukemia cells escape the damage caused by pro-oxidant drugs and develop drug resistance. Hematopoietic stem cells (HSCs) are extremely sensitive to oxidative stress due to their low levels of differentiation, and the use of pro-oxidant drugs inevitably causes damage to HSCs and may even cause severe bone marrow suppression. In this article, we reviewed research progress regarding the generation and regulation of ROS in normal HSCs and ALL cells as well as the impact of ROS on the biological behavior and fate of cells. An in-depth understanding of the regulatory mechanisms of redox homeostasis in normal and malignant HSCs is conducive to the formulation of rational targeted treatment plans to effectively reduce oxidative damage to normal HSCs while eradicating ALL cells.
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spelling doaj.art-74c6f2e7f3094426be802aa2ebc444ab2023-11-21T19:59:55ZengMDPI AGCells2073-44092021-05-01105121810.3390/cells10051218Redox Control in Acute Lymphoblastic Leukemia: From Physiology to Pathology and Therapeutic OpportunitiesYongfeng Chen0Jing Li1Zhiqiang Zhao2Department of Basic Medical Sciences, Medical College of Taizhou University, Taizhou 318000, ChinaDepartment of Histology and Embryology, North Sichuan Medical College, Nanchong 637000, ChinaDepartment of Basic Medical Sciences, Medical College of Taizhou University, Taizhou 318000, ChinaAcute lymphoblastic leukemia (ALL) is a hematological malignancy originating from B- or T-lymphoid progenitor cells. Recent studies have shown that redox dysregulation caused by overproduction of reactive oxygen species (ROS) has an important role in the development and progression of leukemia. The application of pro-oxidant therapy, which targets redox dysregulation, has achieved satisfactory results in alleviating the conditions of and improving the survival rate for patients with ALL. However, drug resistance and side effects are two major challenges that must be addressed in pro-oxidant therapy. Oxidative stress can activate a variety of antioxidant mechanisms to help leukemia cells escape the damage caused by pro-oxidant drugs and develop drug resistance. Hematopoietic stem cells (HSCs) are extremely sensitive to oxidative stress due to their low levels of differentiation, and the use of pro-oxidant drugs inevitably causes damage to HSCs and may even cause severe bone marrow suppression. In this article, we reviewed research progress regarding the generation and regulation of ROS in normal HSCs and ALL cells as well as the impact of ROS on the biological behavior and fate of cells. An in-depth understanding of the regulatory mechanisms of redox homeostasis in normal and malignant HSCs is conducive to the formulation of rational targeted treatment plans to effectively reduce oxidative damage to normal HSCs while eradicating ALL cells.https://www.mdpi.com/2073-4409/10/5/1218acute lymphoblastic leukemiahematopoietic stem cellsROSoxidative stresspro-oxidative therapy
spellingShingle Yongfeng Chen
Jing Li
Zhiqiang Zhao
Redox Control in Acute Lymphoblastic Leukemia: From Physiology to Pathology and Therapeutic Opportunities
Cells
acute lymphoblastic leukemia
hematopoietic stem cells
ROS
oxidative stress
pro-oxidative therapy
title Redox Control in Acute Lymphoblastic Leukemia: From Physiology to Pathology and Therapeutic Opportunities
title_full Redox Control in Acute Lymphoblastic Leukemia: From Physiology to Pathology and Therapeutic Opportunities
title_fullStr Redox Control in Acute Lymphoblastic Leukemia: From Physiology to Pathology and Therapeutic Opportunities
title_full_unstemmed Redox Control in Acute Lymphoblastic Leukemia: From Physiology to Pathology and Therapeutic Opportunities
title_short Redox Control in Acute Lymphoblastic Leukemia: From Physiology to Pathology and Therapeutic Opportunities
title_sort redox control in acute lymphoblastic leukemia from physiology to pathology and therapeutic opportunities
topic acute lymphoblastic leukemia
hematopoietic stem cells
ROS
oxidative stress
pro-oxidative therapy
url https://www.mdpi.com/2073-4409/10/5/1218
work_keys_str_mv AT yongfengchen redoxcontrolinacutelymphoblasticleukemiafromphysiologytopathologyandtherapeuticopportunities
AT jingli redoxcontrolinacutelymphoblasticleukemiafromphysiologytopathologyandtherapeuticopportunities
AT zhiqiangzhao redoxcontrolinacutelymphoblasticleukemiafromphysiologytopathologyandtherapeuticopportunities