Please use this identifier to cite or link to this item: https://ninho.inca.gov.br/jspui/handle/123456789/13764
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dc.contributor.authorPereira, Thais Hancio-
dc.contributor.authorMazzoccoli, Luciano-
dc.contributor.authorGuimarães, Gustavo Henrique Cardoso-
dc.contributor.authorRobaina, Marcela Cristina da Silva-
dc.contributor.authorMendonça, Bruna dos Santos-
dc.contributor.authorMoraes, Gabriela Nestal de-
dc.contributor.authorMonte-Mór, Bárbara da Costa Reis-
dc.contributor.authorGutiyama, Luciana Mayumi-
dc.contributor.authorCarvalho, Luíze Otero de-
dc.contributor.authorDaher Netto, Chaquip-
dc.contributor.authorCosta, Paulo Roberto Ribeiro-
dc.contributor.authorFaria, Fernanda Costas Casal de-
dc.date.accessioned2023-05-11T18:56:12Z-
dc.date.available2023-05-11T18:56:12Z-
dc.date.issued2021-
dc.identifier.citationHANCIO, Thaís et al. The pterocarpanquinone LQB‑118 compound induces apoptosis of cytarabine‑resistant acute myeloid leukemia cells. International Journal Of Oncology, [S.L.], v. 58, n. 6, p. 1-14, mar. 2021.pt_BR
dc.identifier.issn1019-6439 (Impresso)-
dc.identifier.issn1791-2423 (Online)-
dc.identifier.urihttps://ninho.inca.gov.br/jspui/handle/123456789/13764-
dc.descriptionp. 1-14.: il. p&b. e color.pt_BR
dc.description.abstractAcute myeloid leukemia (AML) is a complex hematological disorder characterized by blockage of differentiation and high proliferation rates of myeloid progenitors. Anthracycline and cytarabine‑based therapy has remained the standard treatment for AML over the last four decades. Although this treatment strategy has increased survival rates, patients often develop resistance to these drugs. Despite efforts to understand the mechanisms underlying cytarabine resistance, there have been few advances in the field. The present study developed an in vitro AML cell line model resistant to cytarabine (HL‑60R), and identified chromosomal aberrations by karyotype evaluation and potential molecular mechanisms underlying chemoresistance. Cytarabine decreased cell viability, as determined by MTT assay, and induced cell death and cell cycle arrest in the parental HL‑60 cell line, as revealed by Annexin V/propidium iodide (PI) staining and PI DNA incorporation, respectively, whereas no change was observed in the HL‑60R cell line. In addition, the HL‑60R cell line exhibited a higher tumorigenic capacity in vivo compared with the parental cell line. Notably, no reduction in tumor volume was detected in mice treated with cytarabine and inoculated with HL‑60R cells. In addition, western blotting revealed that the protein expression levels of Bcl‑2, X‑linked inhibitor of apoptosis protein (XIAP) and c‑Myc were upregulated in HL‑60R cells compared with those in HL‑60 cells, along with predominant nuclear localization of the p50 and p65 subunits of NF‑κB in HL‑60R cells. Furthermore, the antitumor effect of LQB‑118 pterocarpanquinone was investigated; this compound induced apoptosis, a reduction in cell viability and a decrease in XIAP expression in cytarabine‑resistant cells. Taken together, these data indicated that acquired cytarabine resistance in AML was a multifactorial process, involving chromosomal aberrations, and differential expression of apoptosis and cell proliferation signaling pathways. Furthermore, LQB‑118 could be a potential alternative therapeutic approach to treat cytarabine‑resistant leukemia cells.pt_BR
dc.language.isoengpt_BR
dc.publisherInternational Journal Of Oncologypt_BR
dc.subjectLeucemia Mieloide Agudapt_BR
dc.subjectLeukemia, Monocytic, Acutept_BR
dc.subjectLeucemia Monocítica Agudapt_BR
dc.subjectCitarabinapt_BR
dc.subjectCytarabinept_BR
dc.subjectResistência a Medicamentospt_BR
dc.subjectDrug Resistancept_BR
dc.subjectResistencia a Medicamentospt_BR
dc.titleThe pterocarpanquinone LQB‑118 compound induces apoptosis of cytarabine‑resistant acute myeloid leukemia cellspt_BR
dc.TypeArticlept_BR
Appears in Collections:Artigos de Periódicos da Pesquisa Experimental e Translacional
Artigos de Periódicos da área de Tecido Ósseo e Conectivo



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