Anti-cancer mechanisms of linalool and 1,8-cineole in non-small cell lung cancer A549 cells

Autores
Rodenak Kladniew, Boris Emilio; Castro, María Agustina; Crespo, Rosana; Galle, Marianela; García de Bravo, Margarita María
Año de publicación
2020
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Linalool and 1,8-cineole are plant-derived isoprenoids with anticancer activities in lung cancer cells, nevertheless, the cellular and molecular mechanisms of action remain poorly understood. The purpose of this study was to determine the anticancer mechanisms of action of linalool and 1,8-cineole in lung adenocarcinoma A549 cells. Linalool (0–2.0 mM) and 1,8-cineole (0–8.0 mM) inhibited cell proliferation by inducing G0/G1 and/or G2/M cell cycle arrest without affecting cell viability of normal lung WI-38 cells. None of the two monoterpenes were able to induce apoptosis, as observed by the lack of caspase-3 and caspase-9 activation, PARP cleavage, and DNA fragmentation. Linalool, but not 1,8-cineole, increased reactive oxygen species production and mitochondrial membrane potential depolarization. Reactive oxygen species were involved in cell growth inhibition and mitochondrial depolarization induced by linalool since the antioxidant N-acetyl-L-cysteine prevented both effects. Besides, linalool (2.0 mM) and 1,8-cineole (8.0 mM) inhibited A549 cell migration. The combination of each monoterpene with simvastatin increased the G0/G1 cell cycle arrest and sensitized cells to apoptosis compared with simvastatin alone. Our results showed that both monoterpenes might be promising anticancer agents with antiproliferative, anti-metastatic, and sensitizer properties for lung cancer therapy.
Instituto de Investigaciones Bioquímicas de La Plata
Materia
Ciencias Médicas
Linalool
1,8-Cineole
Non-small lung cancer cells
Cytostatic effects
Reactive oxygen species
Cell migration
Chemosensitizers
Cell biology
Cell culture
Cytotoxicity
Bioactive plant product
Pharmaceutical science
Natural product
Biochemistry
Oxidative stress
Cancer research
Chemotherapy
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by-nc-nd/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/119509
Acceder
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oai_identifier_str oai:sedici.unlp.edu.ar:10915/119509
network_acronym_str SEDICI
repository_id_str 1329
network_name_str SEDICI (UNLP)
spelling Anti-cancer mechanisms of linalool and 1,8-cineole in non-small cell lung cancer A549 cellsRodenak Kladniew, Boris EmilioCastro, María AgustinaCrespo, RosanaGalle, MarianelaGarcía de Bravo, Margarita MaríaCiencias MédicasLinalool1,8-CineoleNon-small lung cancer cellsCytostatic effectsReactive oxygen speciesCell migrationChemosensitizersCell biologyCell cultureCytotoxicityBioactive plant productPharmaceutical scienceNatural productBiochemistryOxidative stressCancer researchChemotherapyLinalool and 1,8-cineole are plant-derived isoprenoids with anticancer activities in lung cancer cells, nevertheless, the cellular and molecular mechanisms of action remain poorly understood. The purpose of this study was to determine the anticancer mechanisms of action of linalool and 1,8-cineole in lung adenocarcinoma A549 cells. Linalool (0–2.0 mM) and 1,8-cineole (0–8.0 mM) inhibited cell proliferation by inducing G0/G1 and/or G2/M cell cycle arrest without affecting cell viability of normal lung WI-38 cells. None of the two monoterpenes were able to induce apoptosis, as observed by the lack of caspase-3 and caspase-9 activation, PARP cleavage, and DNA fragmentation. Linalool, but not 1,8-cineole, increased reactive oxygen species production and mitochondrial membrane potential depolarization. Reactive oxygen species were involved in cell growth inhibition and mitochondrial depolarization induced by linalool since the antioxidant N-acetyl-L-cysteine prevented both effects. Besides, linalool (2.0 mM) and 1,8-cineole (8.0 mM) inhibited A549 cell migration. The combination of each monoterpene with simvastatin increased the G0/G1 cell cycle arrest and sensitized cells to apoptosis compared with simvastatin alone. Our results showed that both monoterpenes might be promising anticancer agents with antiproliferative, anti-metastatic, and sensitizer properties for lung cancer therapy.Instituto de Investigaciones Bioquímicas de La Plata2020-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttp://sedici.unlp.edu.ar/handle/10915/119509enginfo:eu-repo/semantics/altIdentifier/issn/2405-8440info:eu-repo/semantics/altIdentifier/doi/10.1016/j.heliyon.2020.e05639info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-nd/4.0/Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-03T11:00:20Zoai:sedici.unlp.edu.ar:10915/119509Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-03 11:00:21.049SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Anti-cancer mechanisms of linalool and 1,8-cineole in non-small cell lung cancer A549 cells
title Anti-cancer mechanisms of linalool and 1,8-cineole in non-small cell lung cancer A549 cells
spellingShingle Anti-cancer mechanisms of linalool and 1,8-cineole in non-small cell lung cancer A549 cells
Rodenak Kladniew, Boris Emilio
Ciencias Médicas
Linalool
1,8-Cineole
Non-small lung cancer cells
Cytostatic effects
Reactive oxygen species
Cell migration
Chemosensitizers
Cell biology
Cell culture
Cytotoxicity
Bioactive plant product
Pharmaceutical science
Natural product
Biochemistry
Oxidative stress
Cancer research
Chemotherapy
title_short Anti-cancer mechanisms of linalool and 1,8-cineole in non-small cell lung cancer A549 cells
title_full Anti-cancer mechanisms of linalool and 1,8-cineole in non-small cell lung cancer A549 cells
title_fullStr Anti-cancer mechanisms of linalool and 1,8-cineole in non-small cell lung cancer A549 cells
title_full_unstemmed Anti-cancer mechanisms of linalool and 1,8-cineole in non-small cell lung cancer A549 cells
title_sort Anti-cancer mechanisms of linalool and 1,8-cineole in non-small cell lung cancer A549 cells
dc.creator.none.fl_str_mv Rodenak Kladniew, Boris Emilio
Castro, María Agustina
Crespo, Rosana
Galle, Marianela
García de Bravo, Margarita María
author Rodenak Kladniew, Boris Emilio
author_facet Rodenak Kladniew, Boris Emilio
Castro, María Agustina
Crespo, Rosana
Galle, Marianela
García de Bravo, Margarita María
author_role author
author2 Castro, María Agustina
Crespo, Rosana
Galle, Marianela
García de Bravo, Margarita María
author2_role author
author
author
author
dc.subject.none.fl_str_mv Ciencias Médicas
Linalool
1,8-Cineole
Non-small lung cancer cells
Cytostatic effects
Reactive oxygen species
Cell migration
Chemosensitizers
Cell biology
Cell culture
Cytotoxicity
Bioactive plant product
Pharmaceutical science
Natural product
Biochemistry
Oxidative stress
Cancer research
Chemotherapy
topic Ciencias Médicas
Linalool
1,8-Cineole
Non-small lung cancer cells
Cytostatic effects
Reactive oxygen species
Cell migration
Chemosensitizers
Cell biology
Cell culture
Cytotoxicity
Bioactive plant product
Pharmaceutical science
Natural product
Biochemistry
Oxidative stress
Cancer research
Chemotherapy
dc.description.none.fl_txt_mv Linalool and 1,8-cineole are plant-derived isoprenoids with anticancer activities in lung cancer cells, nevertheless, the cellular and molecular mechanisms of action remain poorly understood. The purpose of this study was to determine the anticancer mechanisms of action of linalool and 1,8-cineole in lung adenocarcinoma A549 cells. Linalool (0–2.0 mM) and 1,8-cineole (0–8.0 mM) inhibited cell proliferation by inducing G0/G1 and/or G2/M cell cycle arrest without affecting cell viability of normal lung WI-38 cells. None of the two monoterpenes were able to induce apoptosis, as observed by the lack of caspase-3 and caspase-9 activation, PARP cleavage, and DNA fragmentation. Linalool, but not 1,8-cineole, increased reactive oxygen species production and mitochondrial membrane potential depolarization. Reactive oxygen species were involved in cell growth inhibition and mitochondrial depolarization induced by linalool since the antioxidant N-acetyl-L-cysteine prevented both effects. Besides, linalool (2.0 mM) and 1,8-cineole (8.0 mM) inhibited A549 cell migration. The combination of each monoterpene with simvastatin increased the G0/G1 cell cycle arrest and sensitized cells to apoptosis compared with simvastatin alone. Our results showed that both monoterpenes might be promising anticancer agents with antiproliferative, anti-metastatic, and sensitizer properties for lung cancer therapy.
Instituto de Investigaciones Bioquímicas de La Plata
description Linalool and 1,8-cineole are plant-derived isoprenoids with anticancer activities in lung cancer cells, nevertheless, the cellular and molecular mechanisms of action remain poorly understood. The purpose of this study was to determine the anticancer mechanisms of action of linalool and 1,8-cineole in lung adenocarcinoma A549 cells. Linalool (0–2.0 mM) and 1,8-cineole (0–8.0 mM) inhibited cell proliferation by inducing G0/G1 and/or G2/M cell cycle arrest without affecting cell viability of normal lung WI-38 cells. None of the two monoterpenes were able to induce apoptosis, as observed by the lack of caspase-3 and caspase-9 activation, PARP cleavage, and DNA fragmentation. Linalool, but not 1,8-cineole, increased reactive oxygen species production and mitochondrial membrane potential depolarization. Reactive oxygen species were involved in cell growth inhibition and mitochondrial depolarization induced by linalool since the antioxidant N-acetyl-L-cysteine prevented both effects. Besides, linalool (2.0 mM) and 1,8-cineole (8.0 mM) inhibited A549 cell migration. The combination of each monoterpene with simvastatin increased the G0/G1 cell cycle arrest and sensitized cells to apoptosis compared with simvastatin alone. Our results showed that both monoterpenes might be promising anticancer agents with antiproliferative, anti-metastatic, and sensitizer properties for lung cancer therapy.
publishDate 2020
dc.date.none.fl_str_mv 2020-12
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
Articulo
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://sedici.unlp.edu.ar/handle/10915/119509
url http://sedici.unlp.edu.ar/handle/10915/119509
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/issn/2405-8440
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.heliyon.2020.e05639
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by-nc-nd/4.0/
Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by-nc-nd/4.0/
Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:SEDICI (UNLP)
instname:Universidad Nacional de La Plata
instacron:UNLP
reponame_str SEDICI (UNLP)
collection SEDICI (UNLP)
instname_str Universidad Nacional de La Plata
instacron_str UNLP
institution UNLP
repository.name.fl_str_mv SEDICI (UNLP) - Universidad Nacional de La Plata
repository.mail.fl_str_mv alira@sedici.unlp.edu.ar
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