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dc.contributor.authorFerreira, Wallax Augusto Silva-
dc.contributor.authorBurbano, Rommel Mario Rodríguez-
dc.contributor.authorPessoa, Claudia do Ó-
dc.contributor.authorHarada, Maria L-
dc.contributor.authorBorges, Bárbara do Nascimento-
dc.contributor.authorOliveira, Edivaldo Herculano Corrêa de-
dc.date.accessioned2020-02-28T17:09:53Z-
dc.date.available2020-02-28T17:09:53Z-
dc.date.issued2020-
dc.identifier.citationFERREIRA, Wallax Augusto Silva et al. Pisosterol induces G2/M cell cycle arrest and apoptosis via the ATM/ATR signaling pathway in human glioma cells. Anti-Cancer Agents in Medicinal Chemistry, v. 20, n.6, p. 734 - 750, 2020.pt_BR
dc.identifier.issn1875-5992-
dc.identifier.urihttp://patua.iec.gov.br//handle/iec/4062-
dc.description.abstractBackground: Pisosterol, a triterpene derived from Pisolithus tinctorius, exhibits potential antitumor activity in various malignancies. However, the molecular mechanisms that mediate the pisosterol-specific effects on glioma cells remain unknown. Objective: This study aimed to evaluate the antitumoral effects of pisosterol on glioma cell lines. Methods: The 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) and trypan blue exclusion assays were used to evaluate the effect of pisosterol on cell proliferation and viability in glioma cells. The effect of pisosterol on the distribution of the cells in cell cycle was performed by flow cytometry. The expression and methylation pattern of the promoter region of MYC, ATM, BCL2, BMI1, CASP3, CDK1, CDKN1A, CDKN2A, CDKN2B, CHEK1, MDM2, p14ARF and TP53 was analyzed by RT-qPCR, western blotting and bisulfite sequencing PCR (BSP-PCR). Results: Here, we reported that pisosterol markedly induced G2/M arrest and apoptosis and decreased the cell viability and proliferation potential of glioma cells in a dose-dependent manner by increasing the expression of ATM, CASP3, CDK1, CDKN1A, CDKN2A, CDKN2B, CHEK1, p14ARF and TP53 and decreasing the expression of MYC, BCL2, BMI1 and MDM2. Pisosterol also triggered both caspase-independent and caspase-dependent apoptotic pathways by regulating the expression of Bcl-2 and activating caspase-3 and p53. Conclusions: We, for the first time, confirmed that the ATM/ATR signaling pathway is a critical mechanism for G2/M arrest in pisosterol-induced glioma cell cycle arrest and suggest that this compound might be a promising anticancer candidate for further investigation.pt_BR
dc.language.isoenpt_BR
dc.language.isoengpt_BR
dc.publisherBentham Science Publisherspt_BR
dc.rightsAcesso Embargadopt_BR
dc.titlePisosterol induces G2/M cell cycle arrest and apoptosis via the ATM/ATR signaling pathway in human glioma cellspt_BR
dc.typeArtigopt_BR
dc.subject.decsPrimaryNeoplasias Encefálicaspt_BR
dc.subject.decsPrimaryNeoplasias Encefálicas / tratamento farmacológicopt_BR
dc.subject.decsPrimaryCiclo Celularpt_BR
dc.subject.decsPrimaryGlioma / tratamento farmacológicopt_BR
dc.subject.decsPrimaryEnsaios de Seleção de Medicamentos Antitumorais / métodospt_BR
dc.subject.decsPrimaryCompostos Químicos / análisept_BR
dc.creator.affilliationMinistério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Laboratório de Cultura de Tecidos e Citogenética Ananindeua, PA, Brasil.pt_BR
dc.creator.affilliationUniversidade Federal do Pará. Instituto de Ciências Biológicas. Laboratório de Citogenética Humana. Belém, PA, Brazil.pt_BR
dc.creator.affilliationUniversidade Federal do Ceará. Departamento de Fisiologia e Farmacologia. Fortaleza, CE, Brazil.pt_BR
dc.creator.affilliationUniversidade Federal do Pará. Instituto de Ciências Biológicas. Laboratório de Biologia Molecular Francisco Mauro Salzano. Belém, PA, Brazil.pt_BR
dc.creator.affilliationUniversidade Federal do Pará. Instituto de Ciências Biológicas. Laboratório de Biologia Molecular Francisco Mauro Salzano. Belém, PA, Brazil.pt_BR
dc.creator.affilliationUniversidade Federal do Pará. Faculdade de Ciências Naturais. Instituto de Ciências Exatas e Naturais. Belém, PA, Brazil.pt_BR
dc.identifier.doi10.2174/1871520620666200203160117-


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