Extracellular lipids of Candida albicans biofilm induce lipid droplet formation and decreased response to a topoisomerase I inhibitor in dysplastic and neoplastic oral cells

Detalhes bibliográficos
Autor(a) principal: Marin-Dett, Freddy Humberto
Data de Publicação: 2023
Outros Autores: Campanella, Jonatas Erick Maimoni, Trovati, Eliane, Bertolini, Maria Célia, Vergani, Carlos Eduardo, Barbugli, Paula Aboud
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Journal of applied oral science (Online)
Texto Completo: https://www.revistas.usp.br/jaos/article/view/207849
Resumo: Objective: Some microorganisms, i.e., Candida albicans, have been associated with cancer onset and development, although whether the fungus promotes cancer or whether cancer facilitates the growth of C. albicans is unclear. In this context, microbial-derived molecules can modulate the growth and resistance of cancer cells. This study isolated extracellular lipids (ECL) from a 36-h Candida albicans biofilm incubated with oral dysplastic (DOK) and neoplastic (SCC 25) cells, which were further challenged with the topoisomerase I inhibitor camptothecin (CPT), a lipophilic anti-tumoral molecule. Methodology: ECL were extracted from a 36-h Candida albicans biofilm with the methanol/chloroform precipitation method and identified with Nuclear Magnetic Resonance (1H-NMR). The MTT tetrazolium assay measured ECL cytotoxicity in DOK and SCC 25 cells, alamarBlue™ assessed cell metabolism, flow cytometry measured cell cycle, and confocal microscopy determined intracellular features. Results: Three major classes of ECL of C. albicans biofilm were found: phosphatidylinositol (PI), phosphatidylcholine (PC), and phosphatidylglycerol (PG). The ECL of C. albicans biofilm had no cytotoxic effect on neither cell after 24 hours, with a tendency to disturb the SCC 25 cell cycle profile (without statistical significance). The ECL-induced intracellular lipid droplet (LD) formation on both cell lines after 72 hours. In this context, ECL enhanced cell metabolism, decreased the response to CPT, and modified intracellular drug distribution. Conclusion:The ECL (PI, PC, and PG) of 36-h Candida albicans biofilm directly interacts with dysplastic and neoplastic oral cells, highlighting the relevance of better understanding C. albicans biofilm signaling in the microenvironment of tumor cells.
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spelling Extracellular lipids of Candida albicans biofilm induce lipid droplet formation and decreased response to a topoisomerase I inhibitor in dysplastic and neoplastic oral cellsCandida albicansBiofilmsLipidsOral cancerObjective: Some microorganisms, i.e., Candida albicans, have been associated with cancer onset and development, although whether the fungus promotes cancer or whether cancer facilitates the growth of C. albicans is unclear. In this context, microbial-derived molecules can modulate the growth and resistance of cancer cells. This study isolated extracellular lipids (ECL) from a 36-h Candida albicans biofilm incubated with oral dysplastic (DOK) and neoplastic (SCC 25) cells, which were further challenged with the topoisomerase I inhibitor camptothecin (CPT), a lipophilic anti-tumoral molecule. Methodology: ECL were extracted from a 36-h Candida albicans biofilm with the methanol/chloroform precipitation method and identified with Nuclear Magnetic Resonance (1H-NMR). The MTT tetrazolium assay measured ECL cytotoxicity in DOK and SCC 25 cells, alamarBlue™ assessed cell metabolism, flow cytometry measured cell cycle, and confocal microscopy determined intracellular features. Results: Three major classes of ECL of C. albicans biofilm were found: phosphatidylinositol (PI), phosphatidylcholine (PC), and phosphatidylglycerol (PG). The ECL of C. albicans biofilm had no cytotoxic effect on neither cell after 24 hours, with a tendency to disturb the SCC 25 cell cycle profile (without statistical significance). The ECL-induced intracellular lipid droplet (LD) formation on both cell lines after 72 hours. In this context, ECL enhanced cell metabolism, decreased the response to CPT, and modified intracellular drug distribution. Conclusion:The ECL (PI, PC, and PG) of 36-h Candida albicans biofilm directly interacts with dysplastic and neoplastic oral cells, highlighting the relevance of better understanding C. albicans biofilm signaling in the microenvironment of tumor cells.Universidade de São Paulo. Faculdade de Odontologia de Bauru2023-02-07info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/jaos/article/view/20784910.1590/1678-7757-2022-0319Journal of Applied Oral Science; Vol. 30 (2022); e20220319Journal of Applied Oral Science; Vol. 30 (2022); e20220319Journal of Applied Oral Science; v. 30 (2022); e202203191678-77651678-7757reponame:Journal of applied oral science (Online)instname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/jaos/article/view/207849/191176Copyright (c) 2023 Journal of Applied Oral Sciencehttp://creativecommons.org/licenses/by/4.0info:eu-repo/semantics/openAccessMarin-Dett, Freddy HumbertoCampanella, Jonatas Erick MaimoniTrovati, ElianeBertolini, Maria CéliaVergani, Carlos EduardoBarbugli, Paula Aboud2023-02-07T13:44:00Zoai:revistas.usp.br:article/207849Revistahttp://www.scielo.br/jaosPUBhttps://www.revistas.usp.br/jaos/oai||jaos@usp.br1678-77651678-7757opendoar:2023-02-07T13:44Journal of applied oral science (Online) - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv Extracellular lipids of Candida albicans biofilm induce lipid droplet formation and decreased response to a topoisomerase I inhibitor in dysplastic and neoplastic oral cells
title Extracellular lipids of Candida albicans biofilm induce lipid droplet formation and decreased response to a topoisomerase I inhibitor in dysplastic and neoplastic oral cells
spellingShingle Extracellular lipids of Candida albicans biofilm induce lipid droplet formation and decreased response to a topoisomerase I inhibitor in dysplastic and neoplastic oral cells
Marin-Dett, Freddy Humberto
Candida albicans
Biofilms
Lipids
Oral cancer
title_short Extracellular lipids of Candida albicans biofilm induce lipid droplet formation and decreased response to a topoisomerase I inhibitor in dysplastic and neoplastic oral cells
title_full Extracellular lipids of Candida albicans biofilm induce lipid droplet formation and decreased response to a topoisomerase I inhibitor in dysplastic and neoplastic oral cells
title_fullStr Extracellular lipids of Candida albicans biofilm induce lipid droplet formation and decreased response to a topoisomerase I inhibitor in dysplastic and neoplastic oral cells
title_full_unstemmed Extracellular lipids of Candida albicans biofilm induce lipid droplet formation and decreased response to a topoisomerase I inhibitor in dysplastic and neoplastic oral cells
title_sort Extracellular lipids of Candida albicans biofilm induce lipid droplet formation and decreased response to a topoisomerase I inhibitor in dysplastic and neoplastic oral cells
author Marin-Dett, Freddy Humberto
author_facet Marin-Dett, Freddy Humberto
Campanella, Jonatas Erick Maimoni
Trovati, Eliane
Bertolini, Maria Célia
Vergani, Carlos Eduardo
Barbugli, Paula Aboud
author_role author
author2 Campanella, Jonatas Erick Maimoni
Trovati, Eliane
Bertolini, Maria Célia
Vergani, Carlos Eduardo
Barbugli, Paula Aboud
author2_role author
author
author
author
author
dc.contributor.author.fl_str_mv Marin-Dett, Freddy Humberto
Campanella, Jonatas Erick Maimoni
Trovati, Eliane
Bertolini, Maria Célia
Vergani, Carlos Eduardo
Barbugli, Paula Aboud
dc.subject.por.fl_str_mv Candida albicans
Biofilms
Lipids
Oral cancer
topic Candida albicans
Biofilms
Lipids
Oral cancer
description Objective: Some microorganisms, i.e., Candida albicans, have been associated with cancer onset and development, although whether the fungus promotes cancer or whether cancer facilitates the growth of C. albicans is unclear. In this context, microbial-derived molecules can modulate the growth and resistance of cancer cells. This study isolated extracellular lipids (ECL) from a 36-h Candida albicans biofilm incubated with oral dysplastic (DOK) and neoplastic (SCC 25) cells, which were further challenged with the topoisomerase I inhibitor camptothecin (CPT), a lipophilic anti-tumoral molecule. Methodology: ECL were extracted from a 36-h Candida albicans biofilm with the methanol/chloroform precipitation method and identified with Nuclear Magnetic Resonance (1H-NMR). The MTT tetrazolium assay measured ECL cytotoxicity in DOK and SCC 25 cells, alamarBlue™ assessed cell metabolism, flow cytometry measured cell cycle, and confocal microscopy determined intracellular features. Results: Three major classes of ECL of C. albicans biofilm were found: phosphatidylinositol (PI), phosphatidylcholine (PC), and phosphatidylglycerol (PG). The ECL of C. albicans biofilm had no cytotoxic effect on neither cell after 24 hours, with a tendency to disturb the SCC 25 cell cycle profile (without statistical significance). The ECL-induced intracellular lipid droplet (LD) formation on both cell lines after 72 hours. In this context, ECL enhanced cell metabolism, decreased the response to CPT, and modified intracellular drug distribution. Conclusion:The ECL (PI, PC, and PG) of 36-h Candida albicans biofilm directly interacts with dysplastic and neoplastic oral cells, highlighting the relevance of better understanding C. albicans biofilm signaling in the microenvironment of tumor cells.
publishDate 2023
dc.date.none.fl_str_mv 2023-02-07
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/jaos/article/view/207849
10.1590/1678-7757-2022-0319
url https://www.revistas.usp.br/jaos/article/view/207849
identifier_str_mv 10.1590/1678-7757-2022-0319
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/jaos/article/view/207849/191176
dc.rights.driver.fl_str_mv Copyright (c) 2023 Journal of Applied Oral Science
http://creativecommons.org/licenses/by/4.0
info:eu-repo/semantics/openAccess
rights_invalid_str_mv Copyright (c) 2023 Journal of Applied Oral Science
http://creativecommons.org/licenses/by/4.0
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Universidade de São Paulo. Faculdade de Odontologia de Bauru
publisher.none.fl_str_mv Universidade de São Paulo. Faculdade de Odontologia de Bauru
dc.source.none.fl_str_mv Journal of Applied Oral Science; Vol. 30 (2022); e20220319
Journal of Applied Oral Science; Vol. 30 (2022); e20220319
Journal of Applied Oral Science; v. 30 (2022); e20220319
1678-7765
1678-7757
reponame:Journal of applied oral science (Online)
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Journal of applied oral science (Online)
collection Journal of applied oral science (Online)
repository.name.fl_str_mv Journal of applied oral science (Online) - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||jaos@usp.br
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