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Use este identificador para citar o ir al link de este elemento: http://hdl.handle.net/1843/77711
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Campo DCValorIdioma
dc.creatorKarin Juliane Pelizzaro Rocha-Britopt_BR
dc.creatorEmanuella Maria Barreto Fonsecapt_BR
dc.creatorBreno Germano de Freitas Oliveirapt_BR
dc.creatorÂngelo de Fátimapt_BR
dc.creatorCarmen Veríssima Ferreira-Halderpt_BR
dc.date.accessioned2024-10-29T22:45:49Z-
dc.date.available2024-10-29T22:45:49Z-
dc.date.issued2020-
dc.citation.volume100pt_BR
dc.citation.spage103881pt_BR
dc.identifier.doihttps://doi.org/10.1016/j.bioorg.2020.103881pt_BR
dc.identifier.issn0045-2068pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/77711-
dc.description.resumoPancreatic cancer is a challenging malignancy, mainly due to aggressive regional involvement, early systemic dissemination, high recurrence rate, and subsequent low patient survival. Scientific advances have contributed in particular by identification of molecular targets as well as the definition of the mechanism of action of the drug candidate in the cellular microenvironment. Previously, we have reported the identification of the molecular mechanisms by which calix[6]arene (CLX6) reduces the viability and proliferation of pancreatic cancer cells. Now, we show the biochemical mechanisms by which CLX6 decreases the aggressiveness of Panc-1 cells, focusing specifically on receptor tyrosine kinases (RTK). The results show that clathrin-mediated endocytosis is involved in CLX6-induced AXL receptor tyrosine kinase degradation in Panc-1 cells. This response may be related to the interaction of CLX6 with the tyrosine kinase receptor binding site (such as AXL). As a result, RTK is internalized and degraded by endocytosis, a condition that negatively impacts events dependent on its signaling. Additionally, CLX6 inhibits migration and invasion of Panc-1 cells by downregulating FAK (downstream mediator of AXL) activity and reducing expression levels of MMP2 and MMP9, directly related to the metastatic profile of these cells. It is noteworthy that according to the mechanism proposed here, CLX6 appears as a candidate to be used in therapeutic protocols of patients that display high expression of AXL and consequently, poor diagnosis.pt_BR
dc.description.sponsorshipFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Geraispt_BR
dc.description.sponsorshipFAPESP - Fundação de Amparo à Pesquisa do Estado de São Paulopt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentICX - DEPARTAMENTO DE QUÍMICApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofBioorganic Chemistrypt_BR
dc.rightsAcesso Restritopt_BR
dc.subjectCalix[6]arenept_BR
dc.subjectPancreatic cancerpt_BR
dc.subjectReceptor tyrosine kinasespt_BR
dc.subjectEndocytosispt_BR
dc.subjectMigrationpt_BR
dc.subject.otherCalixarenospt_BR
dc.subject.otherCancer -Tratamentopt_BR
dc.subject.otherMetástasept_BR
dc.subject.otherCélulas cancerosas - Proliferaçãopt_BR
dc.titleCalix[6]arene diminishes receptor tyrosine kinase lifespan in pancreatic cancer cells and inhibits their migration and invasion efficiencypt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.sciencedirect.com/science/article/pii/S0045206820303138pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-4499-314Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-2344-5590pt_BR
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