한빛사논문
Wonhyoung Seo 1 2 3, Prashanta Silwal 1 2, Ik-Chan Song 4, Eun-Kyeong Jo 5 6 7
1Infection Control Convergence Research Center, Chungnam National University College of Medicine, Daejeon, 35015, Korea.
2Department of Microbiology, Chungnam National University College of Medicine, Daejeon, 35015, Korea.
3Department of Medical Science, Chungnam National University College of Medicine, Daejeon, 35015, Korea.
4Division of Hematology/Oncology, Department of Internal Medicine, Chungnam National University College of Medicine, Daejeon, 35015, Korea.
5Infection Control Convergence Research Center, Chungnam National University College of Medicine, Daejeon, 35015, Korea.
6Department of Microbiology, Chungnam National University College of Medicine, Daejeon, 35015, Korea.
7Department of Medical Science, Chungnam National University College of Medicine, Daejeon, 35015, Korea.
Corresponding author : Eun-Kyeong Jo
Abstract
Acute myeloid leukemia (AML) is a severe hematologic malignancy prevalent in older patients, and the identification of potential therapeutic targets for AML is problematic. Autophagy is a lysosome-dependent catabolic pathway involved in the tumorigenesis and/or treatment of various cancers. Mounting evidence has suggested that autophagy plays a critical role in the initiation and progression of AML and anticancer responses. In this review, we describe recent updates on the multifaceted functions of autophagy linking to genetic alterations of AML. We also summarize the latest evidence for autophagy-related genes as potential prognostic predictors and drivers of AML tumorigenesis. We then discuss the crosstalk between autophagy and tumor cell metabolism into the impact on both AML progression and anti-leukemic treatment. Moreover, a series of autophagy regulators, i.e., the inhibitors and activators, are described as potential therapeutics for AML. Finally, we describe the translation of autophagy-modulating therapeutics into clinical practice. Autophagy in AML is a double-edged sword, necessitating a deeper understanding of how autophagy influences dual functions in AML tumorigenesis and anti-leukemic responses.
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