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Glucose metabolism as a potential therapeutic target in Cytarabine-resistant acute Myeloid leukemia

2024-03-22Research article Open access
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dc.contributor.authorPereira-Vieira, Joana
dc.contributor.authorWeber, Daniela D.
dc.contributor.authorSilva, Sâmia
dc.contributor.authorBarbosa-Matos, Catarina
dc.contributor.authorGranja, Sara
dc.contributor.authorReis, Rui Manuel
dc.contributor.authorQueirós, Odília
dc.contributor.authorKo, Young H.
dc.contributor.authorKofler, Barbara
dc.contributor.authorCasal, Margarida
dc.contributor.authorBaltazar, Fátima
dc.contributor.authorGranja, Sara
dc.date.accessioned2025-06-18T08:41:37Z
dc.date.available2025-06-18T08:41:37Z
dc.date.issued2024-03-22
dc.description.abstractAltered glycolytic metabolism has been associated with chemoresistance in acute myeloid leukemia (AML). However, there are still aspects that need clarification, as well as how to explore these metabolic alterations in therapy. In the present study, we aimed to elucidate the role of glucose metabolism in the acquired resistance of AML cells to cytarabine (Ara-C) and to explore it as a therapeutic target. Resistance was induced by stepwise exposure of AML cells to increasing concentrations of Ara-C. Ara-C-resistant cells were characterized for their growth capacity, genetic alterations, metabolic profile, and sensitivity to different metabolic inhibitors. Ara-C-resistant AML cell lines, KG-1 Ara-R, and MOLM13 Ara-R presented different metabolic profiles. KG-1 Ara-R cells exhibited a more pronounced glycolytic phenotype than parental cells, with a weaker acute response to 3-bromopyruvate (3-BP) but higher sensitivity after 48 h. KG-1 Ara-R cells also display increased respiration rates and are more sensitive to phenformin than parental cells. On the other hand, MOLM13 Ara-R cells display a glucose metabolism profile similar to parental cells, as well as sensitivity to glycolytic inhibitors. These results indicate that acquired resistance to Ara-C in AML may involve metabolic adaptations, which can be explored therapeutically in the AML patient setting who developed resistance to therapy.por
dc.identifier.citationPereira-Vieira, J., Weber, D. D., Silva, S., Barbosa-Matos, C., Granja, S., Reis, R. M., Queirós, O., Ko, Y. H., Kofler, B., Casal, M., & Baltazar, F. (2024). Glucose metabolism as a potential therapeutic target in Cytarabine-resistant acute myeloid leukemia. Pharmaceutics, 16(4), Artigo 4. https://doi.org/10.3390/pharmaceutics16040442
dc.identifier.doi10.3390/pharmaceutics16040442
dc.identifier.eissn1424-8247
dc.identifier.urihttp://hdl.handle.net/10400.22/30157
dc.language.isoeng
dc.peerreviewedyes
dc.publisherMDPI
dc.relationUIDB/50026/2020 and UIDP/50026/2020; NORTE-01-0145-FEDER-000039 and NORTE-01-0145-FEDER-000055; UID/BIA/ 04050/2020; LA/P/0069/2020; SFRH/BD/146065/2019 and SFRH/BD/145955/2019 and COVID/BD/153456/2023
dc.relation.hasversionhttps://www.mdpi.com/1999-4923/16/4/442
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectChemoresistance
dc.subjectCytarabine
dc.subjectAcute myeloid leukemia
dc.subjectMetabolic inhibitors
dc.subjectSeahorse
dc.subjectGlucose metabolism
dc.subject3-bromopyruvate
dc.subjectPhenformin
dc.titleGlucose metabolism as a potential therapeutic target in Cytarabine-resistant acute Myeloid leukemiapor
dc.typeresearch article
dspace.entity.typePublication
oaire.citation.endPage17
oaire.citation.issue4
oaire.citation.startPage2
oaire.citation.titlePharmaceuticals
oaire.citation.volume16
oaire.versionhttp://purl.org/coar/version/c_970fb48d4fbd8a85
person.familyNameGranja
person.givenNameSara
person.identifier.ciencia-idC41F-02E4-065E
person.identifier.orcid0000-0001-8717-6751
relation.isAuthorOfPublication06306a95-9c06-47c7-b2e5-5bbf757bec17
relation.isAuthorOfPublication.latestForDiscovery06306a95-9c06-47c7-b2e5-5bbf757bec17

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