Early-life origin of prostate cancer through deregulation of miR-206 networks in maternally malnourished offspring rats

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MetadadosDescriçãoIdioma
Autor(es): dc.contributorUniversidade Estadual Paulista (UNESP)-
Autor(es): dc.contributorEmory University School of Medicine-
Autor(es): dc.contributorFox Chase Cancer Center-
Autor(es): dc.creatorPortela, Luiz M. F.-
Autor(es): dc.creatorConstantino, Flavia B.-
Autor(es): dc.creatorCamargo, Ana C. L.-
Autor(es): dc.creatorSantos, Sérgio A. A.-
Autor(es): dc.creatorColombelli, Ketlin T.-
Autor(es): dc.creatorFioretto, Matheus N.-
Autor(es): dc.creatorBarata, Luísa A.-
Autor(es): dc.creatorSilva, Erick J. R.-
Autor(es): dc.creatorScarano, Wellerson R.-
Autor(es): dc.creatorFelisbino, Sergio L.-
Autor(es): dc.creatorMoreno, Carlos S.-
Autor(es): dc.creatorJustulin, Luis A.-
Data de aceite: dc.date.accessioned2025-08-21T16:00:37Z-
Data de disponibilização: dc.date.available2025-08-21T16:00:37Z-
Data de envio: dc.date.issued2025-04-29-
Data de envio: dc.date.issued2023-11-30-
Fonte completa do material: dc.identifierhttp://dx.doi.org/10.1038/s41598-023-46068-1-
Fonte completa do material: dc.identifierhttps://hdl.handle.net/11449/304799-
Fonte: dc.identifier.urihttp://educapes.capes.gov.br/handle/11449/304799-
Descrição: dc.descriptionThe Developmental Origins of Health and Disease (DOHaD) concept has provided the framework to assess how early life experiences can shape health and disease throughout the life course. While maternal malnutrition has been proposed as a risk factor for the developmental programming of prostate cancer (PCa), the molecular mechanisms remain poorly understood. Using RNA-seq data, we demonstrated deregulation of miR-206-Plasminogen (PLG) network in the ventral prostate (VP) of young maternally malnourished offspring. RT-qPCR confirmed the deregulation of the miR-206-PLG network in the VP of young and old offspring rats. Considering the key role of estrogenic signaling pathways in prostate carcinogenesis, in vitro miRNA mimic studies also revealed a negative correlation between miR-206 and estrogen receptor α (ESR1) expression in PNT2 cells. Together, we demonstrate that early life estrogenization associated with the deregulation of miR-206 networks can contribute to the developmental origins of PCa in maternally malnourished offspring. Understanding the molecular mechanisms by which early life malnutrition affects offspring health can encourage the adoption of a governmental policy for the prevention of non-communicable chronic diseases related to the DOHaD concept.-
Descrição: dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)-
Descrição: dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)-
Descrição: dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)-
Descrição: dc.descriptionDepartment of Structural and Functional Biology Institute of Biosciences Sao Paulo State University (UNESP), SP-
Descrição: dc.descriptionDepartment of Biophysics and Pharmacology Institute of Biosciences Unesp-
Descrição: dc.descriptionDepartment of Pathology and Laboratory Medicine Emory University School of Medicine-
Descrição: dc.descriptionDepartment of Biomedical Informatics Emory University School of Medicine-
Descrição: dc.descriptionCancer Signaling and Epigenetics Program Fox Chase Cancer Center-
Descrição: dc.descriptionDepartment of Structural and Functional Biology Institute of Biosciences Sao Paulo State University (UNESP), SP-
Descrição: dc.descriptionDepartment of Biophysics and Pharmacology Institute of Biosciences Unesp-
Descrição: dc.descriptionFAPESP: 2017/01063-7-
Descrição: dc.descriptionFAPESP: 2018/26120-6-
Descrição: dc.descriptionCNPq: 310663/2018-0-
Descrição: dc.descriptionCAPES: Finance Code 001-
Idioma: dc.languageen-
Relação: dc.relationScientific Reports-
???dc.source???: dc.sourceScopus-
Título: dc.titleEarly-life origin of prostate cancer through deregulation of miR-206 networks in maternally malnourished offspring rats-
Tipo de arquivo: dc.typelivro digital-
Aparece nas coleções:Repositório Institucional - Unesp

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