Arginine Deprivation in AML Cells Induces Ferroptosis, a Type of Autophagy-Mediated Cell Death

In this study, we showed for the first time that arginine deprivation using a recombinant human arginase induces ferroptosis, an autophagy-mediated type of cell death in AML cells. Acute Myeloid Leukemia (AML) poses significant challenges due to its unfavorable prognosis and limited treatment option...

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محفوظ في:
التفاصيل البيبلوغرافية
المؤلف الرئيسي: Tohme, Sara (author)
التنسيق: masterThesis
منشور في: 2023
الموضوعات:
الوصول للمادة أونلاين:http://hdl.handle.net/10725/15288
https://doi.org/10.26756/th.2023.645
http://libraries.lau.edu.lb/research/laur/terms-of-use/thesis.php
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author Tohme, Sara
author_facet Tohme, Sara
author_role author
dc.creator.none.fl_str_mv Tohme, Sara
dc.date.none.fl_str_mv 2023
2023-07-05
2024-01-23T08:47:48Z
2024-01-23T08:47:48Z
dc.identifier.none.fl_str_mv http://hdl.handle.net/10725/15288
https://doi.org/10.26756/th.2023.645
http://libraries.lau.edu.lb/research/laur/terms-of-use/thesis.php
dc.language.none.fl_str_mv en
dc.publisher.none.fl_str_mv Lebanese American University
dc.rights.*.fl_str_mv info:eu-repo/semantics/openAccess
dc.subject.none.fl_str_mv Acute myeloid leukemia--Treatment
Arginine--Therapeutic use
Cell death
Lebanese American University--Dissertations
Dissertations, Academic
dc.title.none.fl_str_mv Arginine Deprivation in AML Cells Induces Ferroptosis, a Type of Autophagy-Mediated Cell Death
dc.type.none.fl_str_mv Thesis
info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/masterThesis
description In this study, we showed for the first time that arginine deprivation using a recombinant human arginase induces ferroptosis, an autophagy-mediated type of cell death in AML cells. Acute Myeloid Leukemia (AML) poses significant challenges due to its unfavorable prognosis and limited treatment options, particularly in elderly patients. The investigation of arginine depleting enzymes, such as [HuArgI(Co)-PEG5000], has shown promise in selectively inducing cytotoxicity in various cancer cells, including AML. This study aims to explore the cell death mechanism induced by [HuArgI(Co)-PEG5000] and its potential association with ferroptosis, a newly identified iron-dependent form of regulated cell death characterized by ROS accumulation and lipid peroxidation. Our results demonstrate that the cytotoxicity of [HuArgI(Co)-PEG5000] in AML cells leads to the generation of reactive oxygen species (ROS). Scavenging ROS using NAC significantly decreases cell death but has minimal effect on autophagy activation, suggesting that the accumulation of ROS is downstream of autophagy activation but upstream of cell death. This involvement of ROS is confirmed with the gradual increase in intracellular ROS levels, reaching a peak at 48 hours after treatment. This is followed by an increase in lipid peroxidation which peaks at later timepoints and varies between different cell lines. Studying expression levels of regulatory proteins involved in iron homeostasis (FTH1, NCOA4 and DMT1/SLC11A2) and oxidative stress defense (NRF2, KEAP1, AIFM2/FSP1, 4f2hc/CD98, xCT/SLC7A11, and GPX4) suggests altered iron distribution and impaired antioxidant system in treated cells. Overall, these findings provide evidence that arginine deprivation induced by [HuArgI(Co)-PEG5000] leads to increased ROS production, lipid peroxidation, and dysregulation of iron metabolism and antioxidant pathways, all of which are hallmarks for the occurrence of ferroptosis in AML cells following arginine deprivation. Understanding the mechanisms underlying this ferroptotic cell death induced by arginine deprivation may have implications for the development of targeted therapies for AML and other cancer types.
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oai_identifier_str oai:laur.lau.edu.lb:10725/15288
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spelling Arginine Deprivation in AML Cells Induces Ferroptosis, a Type of Autophagy-Mediated Cell DeathTohme, SaraAcute myeloid leukemia--TreatmentArginine--Therapeutic useCell deathLebanese American University--DissertationsDissertations, AcademicIn this study, we showed for the first time that arginine deprivation using a recombinant human arginase induces ferroptosis, an autophagy-mediated type of cell death in AML cells. Acute Myeloid Leukemia (AML) poses significant challenges due to its unfavorable prognosis and limited treatment options, particularly in elderly patients. The investigation of arginine depleting enzymes, such as [HuArgI(Co)-PEG5000], has shown promise in selectively inducing cytotoxicity in various cancer cells, including AML. This study aims to explore the cell death mechanism induced by [HuArgI(Co)-PEG5000] and its potential association with ferroptosis, a newly identified iron-dependent form of regulated cell death characterized by ROS accumulation and lipid peroxidation. Our results demonstrate that the cytotoxicity of [HuArgI(Co)-PEG5000] in AML cells leads to the generation of reactive oxygen species (ROS). Scavenging ROS using NAC significantly decreases cell death but has minimal effect on autophagy activation, suggesting that the accumulation of ROS is downstream of autophagy activation but upstream of cell death. This involvement of ROS is confirmed with the gradual increase in intracellular ROS levels, reaching a peak at 48 hours after treatment. This is followed by an increase in lipid peroxidation which peaks at later timepoints and varies between different cell lines. Studying expression levels of regulatory proteins involved in iron homeostasis (FTH1, NCOA4 and DMT1/SLC11A2) and oxidative stress defense (NRF2, KEAP1, AIFM2/FSP1, 4f2hc/CD98, xCT/SLC7A11, and GPX4) suggests altered iron distribution and impaired antioxidant system in treated cells. Overall, these findings provide evidence that arginine deprivation induced by [HuArgI(Co)-PEG5000] leads to increased ROS production, lipid peroxidation, and dysregulation of iron metabolism and antioxidant pathways, all of which are hallmarks for the occurrence of ferroptosis in AML cells following arginine deprivation. Understanding the mechanisms underlying this ferroptotic cell death induced by arginine deprivation may have implications for the development of targeted therapies for AML and other cancer types.1 online resource (xii, 78 leaves): ill. (some col.)Includes bibliographical references (leaves 64-78)Lebanese American University2024-01-23T08:47:48Z2024-01-23T08:47:48Z20232023-07-05Thesisinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesishttp://hdl.handle.net/10725/15288https://doi.org/10.26756/th.2023.645http://libraries.lau.edu.lb/research/laur/terms-of-use/thesis.phpeninfo:eu-repo/semantics/openAccessoai:laur.lau.edu.lb:10725/152882024-01-23T08:48:56Z
spellingShingle Arginine Deprivation in AML Cells Induces Ferroptosis, a Type of Autophagy-Mediated Cell Death
Tohme, Sara
Acute myeloid leukemia--Treatment
Arginine--Therapeutic use
Cell death
Lebanese American University--Dissertations
Dissertations, Academic
status_str publishedVersion
title Arginine Deprivation in AML Cells Induces Ferroptosis, a Type of Autophagy-Mediated Cell Death
title_full Arginine Deprivation in AML Cells Induces Ferroptosis, a Type of Autophagy-Mediated Cell Death
title_fullStr Arginine Deprivation in AML Cells Induces Ferroptosis, a Type of Autophagy-Mediated Cell Death
title_full_unstemmed Arginine Deprivation in AML Cells Induces Ferroptosis, a Type of Autophagy-Mediated Cell Death
title_short Arginine Deprivation in AML Cells Induces Ferroptosis, a Type of Autophagy-Mediated Cell Death
title_sort Arginine Deprivation in AML Cells Induces Ferroptosis, a Type of Autophagy-Mediated Cell Death
topic Acute myeloid leukemia--Treatment
Arginine--Therapeutic use
Cell death
Lebanese American University--Dissertations
Dissertations, Academic
url http://hdl.handle.net/10725/15288
https://doi.org/10.26756/th.2023.645
http://libraries.lau.edu.lb/research/laur/terms-of-use/thesis.php