Docosahexaenoic acid differentially modulates the cell cycle and metabolism- related genes in tumor and pre-malignant prostate cells

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MetadadosDescriçãoIdioma
Autor(es): dc.contributorUniversidade Estadual de Campinas (UNICAMP)-
Autor(es): dc.contributorUniversidade Estadual Paulista (Unesp)-
Autor(es): dc.creatorTamarindo, Guilherme Henrique-
Autor(es): dc.creatorGoes, Rejane Maira [UNESP]-
Data de aceite: dc.date.accessioned2022-02-22T00:11:39Z-
Data de disponibilização: dc.date.available2022-02-22T00:11:39Z-
Data de envio: dc.date.issued2020-12-09-
Data de envio: dc.date.issued2020-12-09-
Data de envio: dc.date.issued2020-10-01-
Fonte completa do material: dc.identifierhttp://dx.doi.org/10.1016/j.bbalip.2020.158766-
Fonte completa do material: dc.identifierhttp://hdl.handle.net/11449/197233-
Fonte: dc.identifier.urihttp://educapes.capes.gov.br/handle/11449/197233-
Descrição: dc.descriptionProstate cancer (PCa) has different molecular features along progression, including androgen profile, which is associated to therapy inefficiency leading to more aggressive phenotype. Docosahexaenoic acid (DHA) has antiproliferative and pro-apoptotic properties in different cancers associated to cell metabolism modulation. The latter is of particular interest since metabolic reprogramming is one of PCa hallmarks, but is not clear how this occurs among disease progression. Therefore, we evaluated DHA antiproliferative potential in distinct androgenic backgrounds associated to metabolism modulation and androgen-regulated genes. For this purpose, pre-malignant PNT1A and tumor AR-positive 22rv1, and AR-negative PC3 cells were incubated with DHA at 100 mu M-48 h. DHA reduced at least 26% cell number for all lineages due to S-phase decrease in AR-positive and G2/M arrest in AR-negative. Mitochondrial metabolic rate decreased in PNT1A (similar to 38%) and increased in tumor cells (at least 40%). This was associated with ROS overproduction (1.6-fold PNT1A; 2.1 22rv1; 2.2 PC3), lipid accumulation (3-fold PNT1A; 1.8 22rv1; 3.6 PC3) and mitochondria damage in all cell lines. AKT, AMPK and PTEN were not activated in any cell line, but p-ERK1/2 increased (1.5-fold) in PNT1A. Expression of androgen-regulated and nuclear receptors genes showed that DHA affected them in a distinct pattern in each cell line, but most converged to metabolism regulation, response to hormones, lipids and stress. In conclusion, regardless of androgenic or PTEN background DHA exerted antiproliferative effect associated to cell cycle impairment, lipid deregulation and oxidative stress, but differentially regulated gene expression probably due to distinct molecular features of each pathologic stage.-
Descrição: dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)-
Descrição: dc.descriptionSao Jose do Rio Preto Extension and Research Foundation (FAPERP)-
Descrição: dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)-
Descrição: dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)-
Descrição: dc.descriptionUniv Estadual Campinas, Inst Biol, Campinas, SP, Brazil-
Descrição: dc.descriptionSao Paulo State Univ, Inst Biosci Humanities & Exact Sci, Dept Biol, Sao Jose Do Rio Preto, SP, Brazil-
Descrição: dc.descriptionSao Paulo State Univ, Inst Biosci Humanities & Exact Sci, Dept Biol, Sao Jose Do Rio Preto, SP, Brazil-
Descrição: dc.descriptionCAPES: 001-
Descrição: dc.descriptionCAPES: FAPERP - 058/2018-
Descrição: dc.description: 2018/21891-4 FAPESP-
Descrição: dc.description: 311635/2017 CNPq-
Formato: dc.format14-
Idioma: dc.languageen-
Publicador: dc.publisherElsevier B.V.-
Relação: dc.relationBiochimica Et Biophysica Acta-molecular And Cell Biology Of Lipids-
???dc.source???: dc.sourceWeb of Science-
Palavras-chave: dc.subjectProstate cancer-
Palavras-chave: dc.subjectDHA-
Palavras-chave: dc.subjectLipids-
Palavras-chave: dc.subjectMetabolism-
Título: dc.titleDocosahexaenoic acid differentially modulates the cell cycle and metabolism- related genes in tumor and pre-malignant prostate cells-
Tipo de arquivo: dc.typelivro digital-
Aparece nas coleções:Repositório Institucional - Unesp

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