Extracellular lipids of Candida albicans biofilm induce lipid droplet formation and decreased response to a topoisomerase I inhibitor in dysplastic and neoplastic oral cells
Autor(a) principal: | |
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Data de Publicação: | 2023 |
Outros Autores: | , , , , |
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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Journal of applied oral science (Online) |
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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 |
_version_ |
1800221683329531904 |