β-Lapachone and its iodine derivatives cause cell cycle arrest at G2/M phase and reactive oxygen species-mediated apoptosis in human oral squamous cell carcinoma cells

dc.creatorDias, Rosane Borges
dc.creatorAraújo, Taís Bacelar Sacramento de
dc.creatorFreitas, Raíza Dias de
dc.creatorRodrigues, Ana Carolina Borges da Cruz
dc.creatorSousa, Letícia Palmeira
dc.creatorSales, Caroline Brandi Schlaepfer
dc.creatorValverde, Ludmila de Faro
dc.creatorSoares, Milena Botelho Pereira
dc.creatorReis, Mitermayer Galvão dos
dc.creatorColetta, Ricardo Della
dc.creatorRamos, Eduardo Antônio Gonçalves
dc.creatorCamara, Celso Amorim
dc.creatorSilva, Tania Maria Sarmento
dc.creatorBarbosa Filho, José Maria
dc.creatorBezerra, Daniel Pereira
dc.creatorRocha, Clarissa Araújo Gurgel
dc.date2018-09-19T16:30:52Z
dc.date2018-09-19T16:30:52Z
dc.date2018
dc.date.accessioned2023-09-26T20:41:31Z
dc.date.available2023-09-26T20:41:31Z
dc.identifierDIAS, R. B. et al. β-Lapachone and its iodine derivatives cause cell cycle arrest at G2/M phase and reactive oxygen species-mediated apoptosis in human oral squamous cell carcinoma cells. Free Radical Biology and Medicine, v. 126, p. 87–100, 2018.
dc.identifier0891-5849
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/28894
dc.identifier10.1016/j.freeradbiomed.2018.07.022
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8862101
dc.descriptionBrazilian Agencies, Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) and Fundação de Amparo à Pesquisa do Estado da Bahia (FAPESB)
dc.descriptionβ-Lapachone is a natural naphthoquinone originally obtained from the bark of the purple Ipe (Tabebuia avellanedae Lor, Bignoniaceae) and its therapeutic potential in human cancer cells has been evaluated in several studies. In this study, we examined the effects of β-lapachone and its 3-iodine derivatives (3-I-α-lapachone and 3-I-β-lapachone) on cell proliferation, cell death, and cancer-related gene expression in human oral squamous cell carcinoma cells. β-Lapachone and its 3-iodine derivatives showed potent cytotoxicity against different types of human cancer cell lines. Indeed, treatment with these compounds induced cell cycle arrest at G2/M phase, followed by internucleosomal DNA fragmentation, and caused significant increases in phosphatidylserine externalization, caspase-8 and -9 activation, mitochondrial membrane depolarization, reactive oxygen species (ROS) production, and apoptotic cell death morphology. The apoptosis induced by the compounds was prevented by pretreatment with a pan-caspase inhibitor (Z-VAD-FMK) and an antioxidant (N-acetyl-l-cysteine). In vivo, β-lapachone and its 3-iodine derivatives significantly reduced tumor burden and did not alter any of the biochemical, hematological, or histological parameters of the animals. Overall, β-lapachone and its 3-iodine derivatives showed promising cytotoxic activity due to their ability to induce cell cycle arrest at G2/M phase and promote caspase- and ROS-mediated apoptosis. In addition, β-lapachone and its 3-iodine derivatives were able to suppress tumor growth in vivo, indicating that these compounds may be new antitumor drug candidates.
dc.formatapplication/pdf
dc.languageeng
dc.publisherElsevier
dc.rightsopen access
dc.subjectβ-Lapachona
dc.subjectCâncer bucal
dc.subjectQuimioterapia
dc.subjectProdutos naturais
dc.subjectβ-Lapachone
dc.subjectOral cancer
dc.subjectChemotherapy
dc.subjectNatural products
dc.titleβ-Lapachone and its iodine derivatives cause cell cycle arrest at G2/M phase and reactive oxygen species-mediated apoptosis in human oral squamous cell carcinoma cells
dc.typeArticle


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