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Betulinic acid modulates adipocyte differentiation and secretome activity: Downstream effects on Glioblastoma cell migration

2026-05-29Documento de conferência Acesso aberto
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dc.contributor.authorGouveia, Afonso
dc.contributor.authorFerraz, Ricardo
dc.contributor.authorPrudêncio, Cristina
dc.contributor.authorFernandes, Silvia
dc.contributor.authorFernandes, Sílvia
dc.date.accessioned2026-07-28T09:15:17Z
dc.date.available2026-07-28T09:15:17Z
dc.date.issued2026-05-29
dc.description.abstractBetulinic acid (BA) has been recognized for its po-tential to modulate tumor progression and adipocyte function, yet its effects on adipocyte secretome re-modeling and the downstream consequences for glio-blastoma behavior remain incompletely understood1-4. In this study, we investigated the influence of BA on adipocyte secretory activity and its functional impact on glioblastoma cell migration. Direct exposure of U251 glioblastoma cells to BA significantly reduced cell migration, confirming its intrinsic anti-migratory potential. To further explore microenvironmental in-teractions, adipocyte-conditioned media (ACM) de-rived from BA-treated adipocytes was evaluated for its effects on glioblastoma behavior. Secretome anal-ysis demonstrated that BA altered matrix metallopro-teinase (MMP) expression and reduced gelatinolytic activity, indicating significant modulation of extracel-lular matrix–related proteolytic pathways. Functional assessment using wound healing assays revealed that ACM from BA-treated adipocytes did not consistent-ly suppress glioblastoma migration. Intermediate BA concentrations were associated with increased migratory behavior relative to basal conditions, although differences compared with control ACM were not statistically significant. Additionally, transwell migra-tion assays did not demonstrate significant differ-ences between treatment conditions, suggesting that BA-induced alterations in adipocyte secretome com-position do not uniformly translate into measurable changes in glioblastoma migratory capacity across dif-ferent experimental models. These findings indicate that modulation of gelatinolytic pathways alone is insufficient to predict glioblastoma cell migration and support the contribution of additional adipocyte-de-rived signalling mechanisms in regulating tumor be-havior. Overall, BA induces substantial remodelling of adipocyte secretory function, producing complex and non-linear downstream effects on glioblastoma cells. This study highlights the importance of tumor micro-environment crosstalk and underscores the need to evaluate multiple regulatory pathways when consid-ering the therapeutic potential of BA and related bio-active compounds.eng
dc.identifier.citationGouveia, A., Ferraz, R., Prudêncio, C., & Fernandes, S. (2026). Betulinic acid modulates adipocyte differentiation and secretome activity: Downstream effects on Glioblastoma cell migration. Book of Abstracts of the 8th Meeting on Medicinal Biotechnology, 35. https://edicoes.ipp.pt/index.php/books/catalog/book/251
dc.identifier.doi10.26537/ed.p.porto.251
dc.identifier.isbn978-989-9226-20-3
dc.identifier.urihttp://hdl.handle.net/10400.22/32633
dc.language.isoeng
dc.peerreviewedyes
dc.publisherPolitema
dc.relation.hasversionhttps://edicoes.ipp.pt/index.php/books/catalog/book/251
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectBetulinic acid
dc.subjectObesity
dc.subjectGlioblastoma multiforme
dc.titleBetulinic acid modulates adipocyte differentiation and secretome activity: Downstream effects on Glioblastoma cell migrationeng
dc.typeconference object
dspace.entity.typePublication
oaire.citation.conferenceDate2026-05-29
oaire.citation.conferencePlacePorto
oaire.citation.endPage35
oaire.citation.startPage35
oaire.citation.titleBook of Abstracts of the 8th Meeting on Medicinal Biotechnology
oaire.versionhttp://purl.org/coar/version/c_970fb48d4fbd8a85
person.familyNameFernandes
person.givenNameSílvia
person.identifier.ciencia-idFB1A-1376-32B8
person.identifier.orcid0000-0003-2031-0658
person.identifier.scopus-author-id57195931190
relation.isAuthorOfPublicationa15c298e-1ac3-4aac-855c-ec6acbc30e25
relation.isAuthorOfPublication.latestForDiscoverya15c298e-1ac3-4aac-855c-ec6acbc30e25

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