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dc.date.accessioned 2023-11-08T13:12:28Z
dc.date.available 2023-11-08T13:12:28Z
dc.date.issued 2023
dc.identifier.uri http://sedici.unlp.edu.ar/handle/10915/159919
dc.description.abstract Humanin (HN) is a mitochondrial-derived peptide with robust cytoprotective effects in many cell types. Although the administration of HN analogs has been proposed to treat degenerative diseases, its role in the pathogenesis of cancer is poorly understood. Here, we evaluated whether HN affects the chemosensitivity of glioblastoma (GBM) cells. We found that chemotherapy upregulated HN expression in GBM cell lines and primary cultures derived from GBM biopsies. An HN analog (HNGF6A) boosted chemoresistance, increased the migration of GBM cells and improved their capacity to induce endothelial cell migration and proliferation. Chemotherapy also upregulated FPR2 expression, an HN membrane-bound receptor, and the HNGF6A cytoprotective effects were inhibited by an FPR2 receptor antagonist (WRW4). These effects were observed in glioma cells with heterogeneous genetic backgrounds, i.e., glioma cells with wild-type (wtIDH) and mutated (mIDH) isocitrate dehydrogenase. HN silencing using a baculoviral vector that encodes for a specific shRNA for HN (BV.shHN) reduced chemoresistance, and impaired the migration and proangiogenic capacity of GBM cells. Taken together, our findings suggest that HN boosts the hallmark characteristics of GBM, i.e., chemoresistance, migration and endothelial cell proliferation. Thus, strategies that inhibit the HN/FPR2 pathway may improve the response of GBM to standard therapy en
dc.language en es
dc.subject glioblastoma es
dc.subject humanin es
dc.subject FPR2 es
dc.subject chemotherapy es
dc.title Mitochondrial peptide humanin facilitates chemoresistance in glioblastoma cells en
dc.type Articulo es
sedici.identifier.other https://doi.org/10.3390/cancers15164061 es
sedici.identifier.issn 2072-6694 es
sedici.creator.person Peña Agudelo, Jorge A. es
sedici.creator.person Pidre, Matías Luis es
sedici.creator.person García Fallit, Matías es
sedici.creator.person Pérez Küper, Melanie es
sedici.creator.person Zuccato, Camila es
sedici.creator.person Nicola Candia, Alejandro Javier es
sedici.creator.person Marchesini, Abril es
sedici.creator.person Vera, Mariana B. es
sedici.creator.person De Simone, Emilio es
sedici.creator.person Giampaoli, Carla es
sedici.creator.person Amorós Morales, Leslie Cinthya es
sedici.creator.person González, Nazareno es
sedici.creator.person Romanowski, Víctor es
sedici.creator.person Videla-Richardson, Guillermo A. es
sedici.creator.person Seilicovich, Adriana es
sedici.creator.person Candolfi, Marianela es
sedici.subject.materias Biología es
sedici.subject.materias Ciencias Médicas es
sedici.description.fulltext true es
mods.originInfo.place Instituto de Biotecnología y Biología Molecular es
sedici.subtype Articulo es
sedici.rights.license Creative Commons Attribution 4.0 International (CC BY 4.0)
sedici.rights.uri http://creativecommons.org/licenses/by/4.0/
sedici.description.peerReview peer-review es
sedici.relation.journalTitle Cancers es
sedici.relation.journalVolumeAndIssue vol. 15, no. 16 es


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Creative Commons Attribution 4.0 International (CC BY 4.0) Except where otherwise noted, this item's license is described as Creative Commons Attribution 4.0 International (CC BY 4.0)