Loss of glucose 6-phosphate dehydrogenase function increases oxidative stress and glutaminolysis in metastasizing melanoma cells

The pentose phosphate pathway is a major source of NADPH for oxidative stress resistance in cancer cells but there is limited insight into its role in metastasis, when some cancer cells experience high levels of oxidative stress. To address this, we mutated the substrate binding site of glucose 6-ph...

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Veröffentlicht in:Proceedings of the National Academy of Sciences - PNAS 2022-02, Vol.119 (6), p.1-11
Hauptverfasser: Aurora, Arin B., Khivansara, Vishal, Leach, Ashley, Gill, Jennifer G., Martin-Sandoval, Misty, Yang, Chendong, Kasitinon, Stacy Y., Bezwada, Divya, Tasdogan, Alpaslan, Gu, Wen, Mathews, Thomas P., Zhao, Zhiyu, DeBerardinis, Ralph J., Morrison, Sean J.
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container_title Proceedings of the National Academy of Sciences - PNAS
container_volume 119
creator Aurora, Arin B.
Khivansara, Vishal
Leach, Ashley
Gill, Jennifer G.
Martin-Sandoval, Misty
Yang, Chendong
Kasitinon, Stacy Y.
Bezwada, Divya
Tasdogan, Alpaslan
Gu, Wen
Mathews, Thomas P.
Zhao, Zhiyu
DeBerardinis, Ralph J.
Morrison, Sean J.
description The pentose phosphate pathway is a major source of NADPH for oxidative stress resistance in cancer cells but there is limited insight into its role in metastasis, when some cancer cells experience high levels of oxidative stress. To address this, we mutated the substrate binding site of glucose 6-phosphate dehydrogenase (G6PD), which catalyzes the first step of the pentose phosphate pathway, in patient-derived melanomas. G6PD mutant melanomas had significantly decreased G6PD enzymatic activity and depletion of intermediates in the oxidative pentose phosphate pathway. Reduced G6PD function had little effect on the formation of primary subcutaneous tumors, but when these tumors spontaneously metastasized, the frequency of circulating melanoma cells in the blood and metastatic disease burdenwere significantly reduced. G6PD mutant melanomas exhibited increased levels of reactive oxygen species, decreased NADPH levels, and depleted glutathione as compared to control melanomas. G6PD mutant melanomas compensated for this increase in oxidative stress by increasing malic enzyme activity and glutamine consumption. This generated a new metabolic vulnerability as G6PD mutant melanomas were more dependent upon glutaminase than control melanomas, both for oxidative stress management and anaplerosis. The oxidative pentose phosphate pathway, malic enzyme, and glutaminolysis thus confer layered protection against oxidative stress during metastasis.
doi_str_mv 10.1073/pnas.2120617119
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To address this, we mutated the substrate binding site of glucose 6-phosphate dehydrogenase (G6PD), which catalyzes the first step of the pentose phosphate pathway, in patient-derived melanomas. G6PD mutant melanomas had significantly decreased G6PD enzymatic activity and depletion of intermediates in the oxidative pentose phosphate pathway. Reduced G6PD function had little effect on the formation of primary subcutaneous tumors, but when these tumors spontaneously metastasized, the frequency of circulating melanoma cells in the blood and metastatic disease burdenwere significantly reduced. G6PD mutant melanomas exhibited increased levels of reactive oxygen species, decreased NADPH levels, and depleted glutathione as compared to control melanomas. G6PD mutant melanomas compensated for this increase in oxidative stress by increasing malic enzyme activity and glutamine consumption. This generated a new metabolic vulnerability as G6PD mutant melanomas were more dependent upon glutaminase than control melanomas, both for oxidative stress management and anaplerosis. The oxidative pentose phosphate pathway, malic enzyme, and glutaminolysis thus confer layered protection against oxidative stress during metastasis.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.2120617119</identifier><identifier>PMID: 35110412</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Animals ; Binding sites ; Biological Sciences ; Blood circulation ; Cancer ; Dehydrogenase ; Dehydrogenases ; Depletion ; Enzymatic activity ; Enzyme activity ; Enzymes ; Glucose ; Glucose 6 phosphate dehydrogenase ; Glucosephosphate dehydrogenase ; Glucosephosphate Dehydrogenase - metabolism ; Glutaminase ; Glutamine ; Glutamine - metabolism ; Glutathione ; Humans ; Intermediates ; Malic enzyme ; Melanoma ; Melanoma - metabolism ; Metastases ; Metastasis ; Mice ; Mice, Inbred NOD ; Mutants ; NADP - metabolism ; Oxidation resistance ; Oxidation-Reduction ; Oxidative stress ; Oxidative Stress - physiology ; Pentose ; Pentose phosphate pathway ; Pentose Phosphate Pathway - physiology ; Phosphates ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Substrates ; Tumors</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2022-02, Vol.119 (6), p.1-11</ispartof><rights>Copyright © 2022 the Author(s). 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subjects Animals
Binding sites
Biological Sciences
Blood circulation
Cancer
Dehydrogenase
Dehydrogenases
Depletion
Enzymatic activity
Enzyme activity
Enzymes
Glucose
Glucose 6 phosphate dehydrogenase
Glucosephosphate dehydrogenase
Glucosephosphate Dehydrogenase - metabolism
Glutaminase
Glutamine
Glutamine - metabolism
Glutathione
Humans
Intermediates
Malic enzyme
Melanoma
Melanoma - metabolism
Metastases
Metastasis
Mice
Mice, Inbred NOD
Mutants
NADP - metabolism
Oxidation resistance
Oxidation-Reduction
Oxidative stress
Oxidative Stress - physiology
Pentose
Pentose phosphate pathway
Pentose Phosphate Pathway - physiology
Phosphates
Reactive oxygen species
Reactive Oxygen Species - metabolism
Substrates
Tumors
title Loss of glucose 6-phosphate dehydrogenase function increases oxidative stress and glutaminolysis in metastasizing melanoma cells
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