CAVPENET Peptide Inhibits Prostate Cancer Cells Proliferation and Migration through PP1γ-Dependent Inhibition of AKT Signaling

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MetadadosDescriçãoIdioma
Autor(es): dc.contributorUniversity of Aveiro-
Autor(es): dc.contributorPorto Comprehensive Cancer Center Raquel Seruca (Porto.CCC)-
Autor(es): dc.contributorUniversidade Estadual Paulista (UNESP)-
Autor(es): dc.contributorUniversity of Porto-
Autor(es): dc.contributorLaboratory for Integrative and Translational Research in Population Health (ITR)-
Autor(es): dc.contributorBirmingham City University-
Autor(es): dc.creatorMatos, Bárbara-
Autor(es): dc.creatorGomes, Antoniel A. S.-
Autor(es): dc.creatorBernardino, Raquel-
Autor(es): dc.creatorAlves, Marco G.-
Autor(es): dc.creatorHowl, John-
Autor(es): dc.creatorJerónimo, Carmen-
Autor(es): dc.creatorFardilha, Margarida-
Data de aceite: dc.date.accessioned2025-08-21T15:23:53Z-
Data de disponibilização: dc.date.available2025-08-21T15:23:53Z-
Data de envio: dc.date.issued2025-04-29-
Data de envio: dc.date.issued2024-09-01-
Fonte completa do material: dc.identifierhttp://dx.doi.org/10.3390/pharmaceutics16091199-
Fonte completa do material: dc.identifierhttps://hdl.handle.net/11449/298306-
Fonte: dc.identifier.urihttp://educapes.capes.gov.br/handle/11449/298306-
Descrição: dc.descriptionProtein phosphatase 1 (PP1) complexes have emerged as promising targets for anticancer therapies. The ability of peptides to mimic PP1-docking motifs, and so modulate interactions with regulatory factors, has enabled the creation of highly selective modulators of PP1-dependent cellular processes that promote tumor growth. The major objective of this study was to develop a novel bioactive cell-penetrating peptide (bioportide), which, by mimicking the PP1-binding motif of caveolin-1 (CAV1), would regulate PP1 activity, to hinder prostate cancer (PCa) progression. The designed bioportide, herein designated CAVPENET, and a scrambled homologue, were synthesized using microwave-assisted solid-phase methodologies and evaluated using PCa cell lines. Our findings indicate that CAVPENET successfully entered PCa cells to influence both viability and migration. This tumor suppressor activity of CAVPENET was attributed to inhibition of AKT signaling, a consequence of increased PP1γ activity. This led to the suppression of glycolytic metabolism and alteration in lipid metabolism, collectively representing the primary mechanism responsible for the anticancer properties of CAVPENET. Our results underscore the potential of the designed peptide as a novel therapy for PCa patients, setting the stage for further testing in more advanced models to fully realize its therapeutic promise.-
Descrição: dc.descriptionFuel Cell Technologies Program-
Descrição: dc.descriptionFundació Catalana de Trasplantament-
Descrição: dc.descriptionFundação para a Ciência e a Tecnologia-
Descrição: dc.descriptionNuclear Fuel Cycle and Supply Chain-
Descrição: dc.descriptionFaculdade de Ciências e Tecnologia, Universidade Nova de Lisboa-
Descrição: dc.descriptionLaboratory of Signal Transduction Department of Medical Sciences iBiMED-Institute of Biomedicine University of Aveiro-
Descrição: dc.descriptionCancer Biology and Epigenetics Group IPO Porto Research Center (CI-IPOP) RISE@CI-IPOP (Health Research Network) Portuguese Oncology Institute of Porto (IPO Porto) Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), R. Dr. António Bernardino de Almeida-
Descrição: dc.descriptionDepartment of Biophysics & Pharmacology Institute of Biosciences of Botucatu São Paulo State University, SP-
Descrição: dc.descriptionUnit for Multidisciplinary Research in Biomedicine (UMIB) School of Medicine and Biomedical Sciences (ICBAS) University of Porto, Rua Jorge de Viterbo Ferreira 228-
Descrição: dc.descriptionLaboratory for Integrative and Translational Research in Population Health (ITR)-
Descrição: dc.descriptionDepartment of Medical Sciences iBiMED-Institute of Biomedicine University of Aveiro-
Descrição: dc.descriptionFaculty of Health Education and Life Sciences Birmingham City University, Edgbaston-
Descrição: dc.descriptionDepartment of Pathology and Molecular Immunology ICBAS-School of Medicine and Biomedical Sciences University of Porto, Rua de Jorge Viterbo Ferreira, 228-
Descrição: dc.descriptionDepartment of Biophysics & Pharmacology Institute of Biosciences of Botucatu São Paulo State University, SP-
Descrição: dc.descriptionFuel Cell Technologies Program: COVID/BD/153457/2023-
Descrição: dc.descriptionFundació Catalana de Trasplantament: COVID/BD/153457/2023-
Descrição: dc.descriptionFundação para a Ciência e a Tecnologia: COVID/BD/153457/2023-
Descrição: dc.descriptionNuclear Fuel Cycle and Supply Chain: COVID/BD/153457/2023-
Descrição: dc.descriptionFaculdade de Ciências e Tecnologia, Universidade Nova de Lisboa: COVID/BD/153457/2023-
Descrição: dc.descriptionFuel Cell Technologies Program: SFRH/BD/146032/2019-
Descrição: dc.descriptionFundació Catalana de Trasplantament: SFRH/BD/146032/2019-
Descrição: dc.descriptionFundação para a Ciência e a Tecnologia: SFRH/BD/146032/2019-
Descrição: dc.descriptionNuclear Fuel Cycle and Supply Chain: SFRH/BD/146032/2019-
Descrição: dc.descriptionFaculdade de Ciências e Tecnologia, Universidade Nova de Lisboa: SFRH/BD/146032/2019-
Descrição: dc.descriptionFuel Cell Technologies Program: UIDB/04501/2020-
Descrição: dc.descriptionFundació Catalana de Trasplantament: UIDB/04501/2020-
Descrição: dc.descriptionFundação para a Ciência e a Tecnologia: UIDB/04501/2020-
Descrição: dc.descriptionNuclear Fuel Cycle and Supply Chain: UIDB/04501/2020-
Descrição: dc.descriptionFaculdade de Ciências e Tecnologia, Universidade Nova de Lisboa: UIDB/04501/2020-
Idioma: dc.languageen-
Relação: dc.relationPharmaceutics-
???dc.source???: dc.sourceScopus-
Palavras-chave: dc.subjectPP1-targeting peptide-
Palavras-chave: dc.subjectprostate cancer-
Palavras-chave: dc.subjectprotein phosphatase 1-
Palavras-chave: dc.subjectprotein-protein interaction-
Palavras-chave: dc.subjecttreatment-
Título: dc.titleCAVPENET Peptide Inhibits Prostate Cancer Cells Proliferation and Migration through PP1γ-Dependent Inhibition of AKT Signaling-
Tipo de arquivo: dc.typelivro digital-
Aparece nas coleções:Repositório Institucional - Unesp

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