RapamycinFungusV1, Main, Exploration, bibRecord, 000A46

Pharmacological inhibition of fatty-acid oxidation synergistically enhances the effect of l-asparaginase in childhood ALL cells.

Identifieur interne : 000A46 ( Main/Exploration ); précédent : 000A45; suivant : 000A47

Pharmacological inhibition of fatty-acid oxidation synergistically enhances the effect of l-asparaginase in childhood ALL cells.

Source :

Leukemia [ 1476-5551 ] ; 2016.

RBID : pubmed:26239197

Descripteurs français

KwdFr :
- Acides gras (métabolisme), Asparaginase (usage thérapeutique), Autophagie (effets des médicaments et des substances chimiques), Complexe-1 cible mécanistique de la rapamycine (MeSH), Complexes multiprotéiques (physiologie), Humains (MeSH), Leucémie-lymphome lymphoblastique à précurseurs B et T (anatomopathologie), Leucémie-lymphome lymphoblastique à précurseurs B et T (métabolisme), Leucémie-lymphome lymphoblastique à précurseurs B et T (traitement médicamenteux), Lignée cellulaire tumorale (MeSH), Oxydoréduction (MeSH), Protéines G monomériques (physiologie), Pyrimidines (biosynthèse), Sérine-thréonine kinases TOR (physiologie).
MESH :
- anatomopathologie : Leucémie-lymphome lymphoblastique à précurseurs B et T.
- biosynthèse : Pyrimidines.
- effets des médicaments et des substances chimiques : Autophagie.
- métabolisme : Acides gras, Leucémie-lymphome lymphoblastique à précurseurs B et T.
- physiologie : Complexes multiprotéiques, Protéines G monomériques, Sérine-thréonine kinases TOR.
- traitement médicamenteux : Leucémie-lymphome lymphoblastique à précurseurs B et T.
- usage thérapeutique : Asparaginase.
- Complexe-1 cible mécanistique de la rapamycine, Humains, Lignée cellulaire tumorale, Oxydoréduction.

English descriptors

KwdEn :
- Asparaginase (therapeutic use), Autophagy (drug effects), Cell Line, Tumor (MeSH), Fatty Acids (metabolism), Humans (MeSH), Mechanistic Target of Rapamycin Complex 1 (MeSH), Monomeric GTP-Binding Proteins (physiology), Multiprotein Complexes (physiology), Oxidation-Reduction (MeSH), Precursor Cell Lymphoblastic Leukemia-Lymphoma (drug therapy), Precursor Cell Lymphoblastic Leukemia-Lymphoma (metabolism), Precursor Cell Lymphoblastic Leukemia-Lymphoma (pathology), Pyrimidines (biosynthesis), TOR Serine-Threonine Kinases (physiology).
MESH :
- chemical , biosynthesis : Pyrimidines.
- chemical , metabolism : Fatty Acids.
- chemical , physiology : Monomeric GTP-Binding Proteins, Multiprotein Complexes, TOR Serine-Threonine Kinases.
- chemical , therapeutic use : Asparaginase.
- drug effects : Autophagy.
- drug therapy : Precursor Cell Lymphoblastic Leukemia-Lymphoma.
- metabolism : Precursor Cell Lymphoblastic Leukemia-Lymphoma.
- pathology : Precursor Cell Lymphoblastic Leukemia-Lymphoma.
- Cell Line, Tumor, Humans, Mechanistic Target of Rapamycin Complex 1, Oxidation-Reduction.

Abstract

l-asparaginase (ASNase), a key component in the treatment of childhood acute lymphoblastic leukemia (ALL), hydrolyzes plasma asparagine and glutamine and thereby disturbs metabolic homeostasis of leukemic cells. The efficacy of such therapeutic strategy will depend on the capacity of cancer cells to adapt to the metabolic challenge, which could relate to the activation of compensatory metabolic routes. Therefore, we studied the impact of ASNase on the main metabolic pathways in leukemic cells. Treating leukemic cells with ASNase increased fatty-acid oxidation (FAO) and cell respiration and inhibited glycolysis. FAO, together with the decrease in protein translation and pyrimidine synthesis, was positively regulated through inhibition of the RagB-mTORC1 pathway, whereas the effect on glycolysis was RagB-mTORC1 independent. As FAO has been suggested to have a pro-survival function in leukemic cells, we tested its contribution to cell survival following ASNase treatment. Pharmacological inhibition of FAO significantly increased the sensitivity of ALL cells to ASNase. Moreover, constitutive activation of the mammalian target of rapamycin pathway increased apoptosis in leukemic cells treated with ASNase, but did not increase FAO. Our study uncovers a novel therapeutic option based on the combination of ASNase and FAO inhibitors.

DOI: 10.1038/leu.2015.213
PubMed: 26239197

Affiliations:

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<wicri:regionArea>CLIP-Childhood Leukaemia Investigation Prague, Department of Pediatric Hematology/Oncology, Charles University Prague, Prague</wicri:regionArea>
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<affiliation wicri:level="3"><nlm:affiliation>Pôle de Biologie; Hôpital Européen Georges Pompidou; AP-HP, Paris, France.</nlm:affiliation>
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<affiliation wicri:level="3"><nlm:affiliation>Université Paris Descartes; Sorbonne Paris Cité, Paris, France.</nlm:affiliation>
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<author><name sortKey="Carracedo, A" sort="Carracedo, A" uniqKey="Carracedo A" first="A" last="Carracedo">A. Carracedo</name>
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<country xml:lang="fr">Espagne</country>
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<affiliation wicri:level="1"><nlm:affiliation>Ikerbasque, Basque Foundation for Science, Bilbao, Spain.</nlm:affiliation>
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<affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular biology, University of the Basque Country, Leioa, Spain.</nlm:affiliation>
<country xml:lang="fr">Espagne</country>
<wicri:regionArea>Department of Biochemistry and Molecular biology, University of the Basque Country, Leioa</wicri:regionArea>
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<author><name sortKey="Trka, J" sort="Trka, J" uniqKey="Trka J" first="J" last="Trka">J. Trka</name>
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<country xml:lang="fr">République tchèque</country>
<wicri:regionArea>CLIP-Childhood Leukaemia Investigation Prague, Department of Pediatric Hematology/Oncology, Charles University Prague, Prague</wicri:regionArea>
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<affiliation wicri:level="3"><nlm:affiliation>University Hospital Motol, Prague, Czech Republic.</nlm:affiliation>
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<wicri:regionArea>University Hospital Motol, Prague</wicri:regionArea>
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</placeName>
</affiliation>
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<author><name sortKey="Starkova, J" sort="Starkova, J" uniqKey="Starkova J" first="J" last="Starkova">J. Starkova</name>
<affiliation wicri:level="3"><nlm:affiliation>CLIP-Childhood Leukaemia Investigation Prague, Department of Pediatric Hematology/Oncology, Charles University Prague, Prague, Czech Republic.</nlm:affiliation>
<country xml:lang="fr">République tchèque</country>
<wicri:regionArea>CLIP-Childhood Leukaemia Investigation Prague, Department of Pediatric Hematology/Oncology, Charles University Prague, Prague</wicri:regionArea>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Pharmacological inhibition of fatty-acid oxidation synergistically enhances the effect of l-asparaginase in childhood ALL cells.</title>
<author><name sortKey="Hermanova, I" sort="Hermanova, I" uniqKey="Hermanova I" first="I" last="Hermanova">I. Hermanova</name>
<affiliation wicri:level="3"><nlm:affiliation>CLIP-Childhood Leukaemia Investigation Prague, Department of Pediatric Hematology/Oncology, Charles University Prague, Prague, Czech Republic.</nlm:affiliation>
<country xml:lang="fr">République tchèque</country>
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<author><name sortKey="Arruabarrena Aristorena, A" sort="Arruabarrena Aristorena, A" uniqKey="Arruabarrena Aristorena A" first="A" last="Arruabarrena-Aristorena">A. Arruabarrena-Aristorena</name>
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<country xml:lang="fr">Espagne</country>
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<author><name sortKey="Valis, K" sort="Valis, K" uniqKey="Valis K" first="K" last="Valis">K. Valis</name>
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<affiliation wicri:level="3"><nlm:affiliation>Department of Biochemistry, Charles University, Prague, Czech Republic.</nlm:affiliation>
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<wicri:regionArea>Department of Biochemistry, Charles University, Prague</wicri:regionArea>
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<author><name sortKey="Nuskova, H" sort="Nuskova, H" uniqKey="Nuskova H" first="H" last="Nuskova">H. Nuskova</name>
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<country xml:lang="fr">République tchèque</country>
<wicri:regionArea>Department of Bioenergetics, Institute of Physiology of the Czech Academy of Sciences, Prague</wicri:regionArea>
<placeName><settlement type="city">Prague</settlement>
<region type="région" nuts="2">Bohême centrale</region>
</placeName>
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<author><name sortKey="Alberich Jorda, M" sort="Alberich Jorda, M" uniqKey="Alberich Jorda M" first="M" last="Alberich-Jorda">M. Alberich-Jorda</name>
<affiliation wicri:level="3"><nlm:affiliation>Laboratory of Molecular Immunology, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.</nlm:affiliation>
<country xml:lang="fr">République tchèque</country>
<wicri:regionArea>Laboratory of Molecular Immunology, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague</wicri:regionArea>
<placeName><settlement type="city">Prague</settlement>
<region type="région" nuts="2">Bohême centrale</region>
</placeName>
</affiliation>
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<author><name sortKey="Fiser, K" sort="Fiser, K" uniqKey="Fiser K" first="K" last="Fiser">K. Fiser</name>
<affiliation wicri:level="3"><nlm:affiliation>CLIP-Childhood Leukaemia Investigation Prague, Department of Pediatric Hematology/Oncology, Charles University Prague, Prague, Czech Republic.</nlm:affiliation>
<country xml:lang="fr">République tchèque</country>
<wicri:regionArea>CLIP-Childhood Leukaemia Investigation Prague, Department of Pediatric Hematology/Oncology, Charles University Prague, Prague</wicri:regionArea>
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<author><name sortKey="Fernandez Ruiz, S" sort="Fernandez Ruiz, S" uniqKey="Fernandez Ruiz S" first="S" last="Fernandez-Ruiz">S. Fernandez-Ruiz</name>
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<author><name sortKey="Kavan, D" sort="Kavan, D" uniqKey="Kavan D" first="D" last="Kavan">D. Kavan</name>
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<region type="région" nuts="2">Bohême centrale</region>
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<affiliation wicri:level="3"><nlm:affiliation>Department of Biochemistry, Charles University, Prague, Czech Republic.</nlm:affiliation>
<country xml:lang="fr">République tchèque</country>
<wicri:regionArea>Department of Biochemistry, Charles University, Prague</wicri:regionArea>
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<author><name sortKey="Pecinova, A" sort="Pecinova, A" uniqKey="Pecinova A" first="A" last="Pecinova">A. Pecinova</name>
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<country xml:lang="fr">République tchèque</country>
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<author><name sortKey="Niso Santano, M" sort="Niso Santano, M" uniqKey="Niso Santano M" first="M" last="Niso-Santano">M. Niso-Santano</name>
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<country xml:lang="fr">France</country>
<wicri:regionArea>Equipe 11 labellisée par la Ligue Nationale Contre le Cancer; INSERM U1138; Centre de Recherche des Cordeliers, Paris</wicri:regionArea>
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<region type="old region">Île-de-France</region>
<settlement type="city">Paris</settlement>
</placeName>
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<affiliation wicri:level="3"><nlm:affiliation>Metabolomics and Molecular Cell Biology Platforms; Gustave Roussy, Villejuif, France.</nlm:affiliation>
<country xml:lang="fr">France</country>
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</placeName>
</affiliation>
</author>
<author><name sortKey="Zaliova, M" sort="Zaliova, M" uniqKey="Zaliova M" first="M" last="Zaliova">M. Zaliova</name>
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<country xml:lang="fr">République tchèque</country>
<wicri:regionArea>CLIP-Childhood Leukaemia Investigation Prague, Department of Pediatric Hematology/Oncology, Charles University Prague, Prague</wicri:regionArea>
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</placeName>
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</author>
<author><name sortKey="Novak, P" sort="Novak, P" uniqKey="Novak P" first="P" last="Novak">P. Novak</name>
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<region type="région" nuts="2">Bohême centrale</region>
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<affiliation wicri:level="3"><nlm:affiliation>Department of Biochemistry, Charles University, Prague, Czech Republic.</nlm:affiliation>
<country xml:lang="fr">République tchèque</country>
<wicri:regionArea>Department of Biochemistry, Charles University, Prague</wicri:regionArea>
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</placeName>
</affiliation>
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<author><name sortKey="Houstek, J" sort="Houstek, J" uniqKey="Houstek J" first="J" last="Houstek">J. Houstek</name>
<affiliation wicri:level="3"><nlm:affiliation>Department of Bioenergetics, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic.</nlm:affiliation>
<country xml:lang="fr">République tchèque</country>
<wicri:regionArea>Department of Bioenergetics, Institute of Physiology of the Czech Academy of Sciences, Prague</wicri:regionArea>
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</placeName>
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<author><name sortKey="Mracek, T" sort="Mracek, T" uniqKey="Mracek T" first="T" last="Mracek">T. Mracek</name>
<affiliation wicri:level="3"><nlm:affiliation>Department of Bioenergetics, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic.</nlm:affiliation>
<country xml:lang="fr">République tchèque</country>
<wicri:regionArea>Department of Bioenergetics, Institute of Physiology of the Czech Academy of Sciences, Prague</wicri:regionArea>
<placeName><settlement type="city">Prague</settlement>
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<author><name sortKey="Kroemer, G" sort="Kroemer, G" uniqKey="Kroemer G" first="G" last="Kroemer">G. Kroemer</name>
<affiliation wicri:level="3"><nlm:affiliation>Equipe 11 labellisée par la Ligue Nationale Contre le Cancer; INSERM U1138; Centre de Recherche des Cordeliers, Paris, France.</nlm:affiliation>
<country xml:lang="fr">France</country>
<wicri:regionArea>Equipe 11 labellisée par la Ligue Nationale Contre le Cancer; INSERM U1138; Centre de Recherche des Cordeliers, Paris</wicri:regionArea>
<placeName><region type="region">Île-de-France</region>
<region type="old region">Île-de-France</region>
<settlement type="city">Paris</settlement>
</placeName>
</affiliation>
<affiliation wicri:level="3"><nlm:affiliation>Metabolomics and Molecular Cell Biology Platforms; Gustave Roussy, Villejuif, France.</nlm:affiliation>
<country xml:lang="fr">France</country>
<wicri:regionArea>Metabolomics and Molecular Cell Biology Platforms; Gustave Roussy, Villejuif</wicri:regionArea>
<placeName><settlement type="city">Villejuif</settlement>
</placeName>
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<affiliation wicri:level="3"><nlm:affiliation>Pôle de Biologie; Hôpital Européen Georges Pompidou; AP-HP, Paris, France.</nlm:affiliation>
<country xml:lang="fr">France</country>
<wicri:regionArea>Pôle de Biologie; Hôpital Européen Georges Pompidou; AP-HP, Paris</wicri:regionArea>
<placeName><region type="region">Île-de-France</region>
<region type="old region">Île-de-France</region>
<settlement type="city">Paris</settlement>
</placeName>
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<affiliation wicri:level="3"><nlm:affiliation>Université Paris Descartes; Sorbonne Paris Cité, Paris, France.</nlm:affiliation>
<country xml:lang="fr">France</country>
<wicri:regionArea>Université Paris Descartes; Sorbonne Paris Cité, Paris</wicri:regionArea>
<placeName><region type="region">Île-de-France</region>
<region type="old region">Île-de-France</region>
<settlement type="city">Paris</settlement>
</placeName>
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<author><name sortKey="Carracedo, A" sort="Carracedo, A" uniqKey="Carracedo A" first="A" last="Carracedo">A. Carracedo</name>
<affiliation wicri:level="1"><nlm:affiliation>CIC bioGUNE Technology Park of Bizkaia, Derio, Spain.</nlm:affiliation>
<country xml:lang="fr">Espagne</country>
<wicri:regionArea>CIC bioGUNE Technology Park of Bizkaia, Derio</wicri:regionArea>
<wicri:noRegion>Derio</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Ikerbasque, Basque Foundation for Science, Bilbao, Spain.</nlm:affiliation>
<country xml:lang="fr">Espagne</country>
<wicri:regionArea>Ikerbasque, Basque Foundation for Science, Bilbao</wicri:regionArea>
<wicri:noRegion>Bilbao</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry and Molecular biology, University of the Basque Country, Leioa, Spain.</nlm:affiliation>
<country xml:lang="fr">Espagne</country>
<wicri:regionArea>Department of Biochemistry and Molecular biology, University of the Basque Country, Leioa</wicri:regionArea>
<wicri:noRegion>Leioa</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Trka, J" sort="Trka, J" uniqKey="Trka J" first="J" last="Trka">J. Trka</name>
<affiliation wicri:level="3"><nlm:affiliation>CLIP-Childhood Leukaemia Investigation Prague, Department of Pediatric Hematology/Oncology, Charles University Prague, Prague, Czech Republic.</nlm:affiliation>
<country xml:lang="fr">République tchèque</country>
<wicri:regionArea>CLIP-Childhood Leukaemia Investigation Prague, Department of Pediatric Hematology/Oncology, Charles University Prague, Prague</wicri:regionArea>
<placeName><settlement type="city">Prague</settlement>
<region type="région" nuts="2">Bohême centrale</region>
</placeName>
</affiliation>
<affiliation wicri:level="3"><nlm:affiliation>University Hospital Motol, Prague, Czech Republic.</nlm:affiliation>
<country xml:lang="fr">République tchèque</country>
<wicri:regionArea>University Hospital Motol, Prague</wicri:regionArea>
<placeName><settlement type="city">Prague</settlement>
<region type="région" nuts="2">Bohême centrale</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Starkova, J" sort="Starkova, J" uniqKey="Starkova J" first="J" last="Starkova">J. Starkova</name>
<affiliation wicri:level="3"><nlm:affiliation>CLIP-Childhood Leukaemia Investigation Prague, Department of Pediatric Hematology/Oncology, Charles University Prague, Prague, Czech Republic.</nlm:affiliation>
<country xml:lang="fr">République tchèque</country>
<wicri:regionArea>CLIP-Childhood Leukaemia Investigation Prague, Department of Pediatric Hematology/Oncology, Charles University Prague, Prague</wicri:regionArea>
<placeName><settlement type="city">Prague</settlement>
<region type="région" nuts="2">Bohême centrale</region>
</placeName>
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<series><title level="j">Leukemia</title>
<idno type="eISSN">1476-5551</idno>
<imprint><date when="2016" type="published">2016</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Asparaginase (therapeutic use)</term>
<term>Autophagy (drug effects)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Fatty Acids (metabolism)</term>
<term>Humans (MeSH)</term>
<term>Mechanistic Target of Rapamycin Complex 1 (MeSH)</term>
<term>Monomeric GTP-Binding Proteins (physiology)</term>
<term>Multiprotein Complexes (physiology)</term>
<term>Oxidation-Reduction (MeSH)</term>
<term>Precursor Cell Lymphoblastic Leukemia-Lymphoma (drug therapy)</term>
<term>Precursor Cell Lymphoblastic Leukemia-Lymphoma (metabolism)</term>
<term>Precursor Cell Lymphoblastic Leukemia-Lymphoma (pathology)</term>
<term>Pyrimidines (biosynthesis)</term>
<term>TOR Serine-Threonine Kinases (physiology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Acides gras (métabolisme)</term>
<term>Asparaginase (usage thérapeutique)</term>
<term>Autophagie (effets des médicaments et des substances chimiques)</term>
<term>Complexe-1 cible mécanistique de la rapamycine (MeSH)</term>
<term>Complexes multiprotéiques (physiologie)</term>
<term>Humains (MeSH)</term>
<term>Leucémie-lymphome lymphoblastique à précurseurs B et T (anatomopathologie)</term>
<term>Leucémie-lymphome lymphoblastique à précurseurs B et T (métabolisme)</term>
<term>Leucémie-lymphome lymphoblastique à précurseurs B et T (traitement médicamenteux)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Oxydoréduction (MeSH)</term>
<term>Protéines G monomériques (physiologie)</term>
<term>Pyrimidines (biosynthèse)</term>
<term>Sérine-thréonine kinases TOR (physiologie)</term>
</keywords>
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</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Fatty Acids</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Monomeric GTP-Binding Proteins</term>
<term>Multiprotein Complexes</term>
<term>TOR Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Asparaginase</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Leucémie-lymphome lymphoblastique à précurseurs B et T</term>
</keywords>
<keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Pyrimidines</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Precursor Cell Lymphoblastic Leukemia-Lymphoma</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Autophagie</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Precursor Cell Lymphoblastic Leukemia-Lymphoma</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Acides gras</term>
<term>Leucémie-lymphome lymphoblastique à précurseurs B et T</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Precursor Cell Lymphoblastic Leukemia-Lymphoma</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Complexes multiprotéiques</term>
<term>Protéines G monomériques</term>
<term>Sérine-thréonine kinases TOR</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Leucémie-lymphome lymphoblastique à précurseurs B et T</term>
</keywords>
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</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term>
<term>Humans</term>
<term>Mechanistic Target of Rapamycin Complex 1</term>
<term>Oxidation-Reduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Complexe-1 cible mécanistique de la rapamycine</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Oxydoréduction</term>
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<front><div type="abstract" xml:lang="en">l-asparaginase (ASNase), a key component in the treatment of childhood acute lymphoblastic leukemia (ALL), hydrolyzes plasma asparagine and glutamine and thereby disturbs metabolic homeostasis of leukemic cells. The efficacy of such therapeutic strategy will depend on the capacity of cancer cells to adapt to the metabolic challenge, which could relate to the activation of compensatory metabolic routes. Therefore, we studied the impact of ASNase on the main metabolic pathways in leukemic cells. Treating leukemic cells with ASNase increased fatty-acid oxidation (FAO) and cell respiration and inhibited glycolysis. FAO, together with the decrease in protein translation and pyrimidine synthesis, was positively regulated through inhibition of the RagB-mTORC1 pathway, whereas the effect on glycolysis was RagB-mTORC1 independent. As FAO has been suggested to have a pro-survival function in leukemic cells, we tested its contribution to cell survival following ASNase treatment. Pharmacological inhibition of FAO significantly increased the sensitivity of ALL cells to ASNase. Moreover, constitutive activation of the mammalian target of rapamycin pathway increased apoptosis in leukemic cells treated with ASNase, but did not increase FAO. Our study uncovers a novel therapeutic option based on the combination of ASNase and FAO inhibitors. </div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26239197</PMID>
<DateCompleted><Year>2016</Year>
<Month>06</Month>
<Day>01</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1476-5551</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>30</Volume>
<Issue>1</Issue>
<PubDate><Year>2016</Year>
<Month>Jan</Month>
</PubDate>
</JournalIssue>
<Title>Leukemia</Title>
<ISOAbbreviation>Leukemia</ISOAbbreviation>
</Journal>
<ArticleTitle>Pharmacological inhibition of fatty-acid oxidation synergistically enhances the effect of l-asparaginase in childhood ALL cells.</ArticleTitle>
<Pagination><MedlinePgn>209-18</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1038/leu.2015.213</ELocationID>
<Abstract><AbstractText>l-asparaginase (ASNase), a key component in the treatment of childhood acute lymphoblastic leukemia (ALL), hydrolyzes plasma asparagine and glutamine and thereby disturbs metabolic homeostasis of leukemic cells. The efficacy of such therapeutic strategy will depend on the capacity of cancer cells to adapt to the metabolic challenge, which could relate to the activation of compensatory metabolic routes. Therefore, we studied the impact of ASNase on the main metabolic pathways in leukemic cells. Treating leukemic cells with ASNase increased fatty-acid oxidation (FAO) and cell respiration and inhibited glycolysis. FAO, together with the decrease in protein translation and pyrimidine synthesis, was positively regulated through inhibition of the RagB-mTORC1 pathway, whereas the effect on glycolysis was RagB-mTORC1 independent. As FAO has been suggested to have a pro-survival function in leukemic cells, we tested its contribution to cell survival following ASNase treatment. Pharmacological inhibition of FAO significantly increased the sensitivity of ALL cells to ASNase. Moreover, constitutive activation of the mammalian target of rapamycin pathway increased apoptosis in leukemic cells treated with ASNase, but did not increase FAO. Our study uncovers a novel therapeutic option based on the combination of ASNase and FAO inhibitors. </AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hermanova</LastName>
<ForeName>I</ForeName>
<Initials>I</Initials>
<AffiliationInfo><Affiliation>CLIP-Childhood Leukaemia Investigation Prague, Department of Pediatric Hematology/Oncology, Charles University Prague, Prague, Czech Republic.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Arruabarrena-Aristorena</LastName>
<ForeName>A</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>CIC bioGUNE Technology Park of Bizkaia, Derio, Spain.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Valis</LastName>
<ForeName>K</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Laboratory of Structural Biology and Cell Signaling, Institute of Microbiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Biochemistry, Charles University, Prague, Czech Republic.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Nuskova</LastName>
<ForeName>H</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Bioenergetics, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Alberich-Jorda</LastName>
<ForeName>M</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Laboratory of Molecular Immunology, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fiser</LastName>
<ForeName>K</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>CLIP-Childhood Leukaemia Investigation Prague, Department of Pediatric Hematology/Oncology, Charles University Prague, Prague, Czech Republic.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fernandez-Ruiz</LastName>
<ForeName>S</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>CIC bioGUNE Technology Park of Bizkaia, Derio, Spain.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kavan</LastName>
<ForeName>D</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Laboratory of Structural Biology and Cell Signaling, Institute of Microbiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Biochemistry, Charles University, Prague, Czech Republic.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pecinova</LastName>
<ForeName>A</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Bioenergetics, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Niso-Santano</LastName>
<ForeName>M</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Equipe 11 labellisée par la Ligue Nationale Contre le Cancer; INSERM U1138; Centre de Recherche des Cordeliers, Paris, France.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Metabolomics and Molecular Cell Biology Platforms; Gustave Roussy, Villejuif, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zaliova</LastName>
<ForeName>M</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>CLIP-Childhood Leukaemia Investigation Prague, Department of Pediatric Hematology/Oncology, Charles University Prague, Prague, Czech Republic.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Novak</LastName>
<ForeName>P</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Laboratory of Structural Biology and Cell Signaling, Institute of Microbiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Biochemistry, Charles University, Prague, Czech Republic.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Houstek</LastName>
<ForeName>J</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Bioenergetics, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mracek</LastName>
<ForeName>T</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Department of Bioenergetics, Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kroemer</LastName>
<ForeName>G</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Equipe 11 labellisée par la Ligue Nationale Contre le Cancer; INSERM U1138; Centre de Recherche des Cordeliers, Paris, France.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Metabolomics and Molecular Cell Biology Platforms; Gustave Roussy, Villejuif, France.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Pôle de Biologie; Hôpital Européen Georges Pompidou; AP-HP, Paris, France.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Université Paris Descartes; Sorbonne Paris Cité, Paris, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Carracedo</LastName>
<ForeName>A</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>CIC bioGUNE Technology Park of Bizkaia, Derio, Spain.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Ikerbasque, Basque Foundation for Science, Bilbao, Spain.</Affiliation>
</AffiliationInfo>
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	Serveur d'exploration sur la rapamycine et les champignons
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Pharmacological inhibition of fatty-acid oxidation synergistically enhances the effect of l-asparaginase in childhood ALL cells.

Pharmacological inhibition of fatty-acid oxidation synergistically enhances the effect of l-asparaginase in childhood ALL cells.

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