Autophagy and mitochondrial metabolism: insights into their role and therapeutic potential in chronic myeloid leukaemia

被引：14
作者：
Baquero, Pablo [1 ]
Dawson, Amy [1 ]
Helgason, Gudmundur Vignir [1 ,2 ]
机构：
[1] Univ Glasgow, Inst Canc Sci, Wolfson Wohl Canc Res Ctr, Glasgow G61 1QH, Lanark, Scotland
[2] Univ Glasgow, Inst Canc Sci, Paul OGorman Leukemia Res Ctr, Glasgow, Lanark, Scotland
来源：
FEBS JOURNAL | 2019年 / 286卷 / 07期
关键词：
autophagy; chronic myeloid leukaemia; metabolism; mitochondria; oxidative phosphorylation; therapeutics; CHRONIC MYELOGENOUS LEUKEMIA; HEMATOPOIETIC STEM-CELLS; KINASE INHIBITORS; INITIATING CELLS; CHRONIC-PHASE; HYDROXYCHLOROQUINE; RESISTANCE; IMATINIB; GROWTH; BIOGENESIS;
D O I：
10.1111/febs.14659
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Despite the development of selective BCR-ABL-targeting tyrosine kinase inhibitors (TKIs) transforming the management of chronic myeloid leukaemia (CML), therapy-resistant leukaemic stem cells (LSCs) persist after TKI treatment and present an obstacle to a CML cure. Recently, we and others have made significant contributions to the field by unravelling survival dependencies in LSCs to work towards the goal of eradicating LSCs in CML patients. In this review, we describe these findings focusing on autophagy and mitochondrial metabolism, which have recently been uncovered as two essential processes for LSCs quiescence and survival respectively. In addition, we discuss the therapeutic potential of autophagy and mitochondrial metabolism inhibition as a strategy to eliminate CML cells in patients where the resistance to TKI is driven by BCR-ABL-independent mechanism(s).
引用
收藏
页码：1271 / 1283
页数：13
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