Propranolol inhibits cell viability and expression of the pro-tumorigenic proteins Akt, NF-ĸB, and VEGF in oral squamous cell carcinoma

Detalhes bibliográficos
Autor(a) principal: Shibuya, Caroline Miho [UNESP]
Data de Publicação: 2022
Outros Autores: Tjioe, Kellen Cristine [UNESP], Oliveira, Sandra Helena Penha [UNESP], Bernabé, Daniel Galera [UNESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://dx.doi.org/10.1016/j.archoralbio.2022.105383
http://hdl.handle.net/11449/230479
Resumo: Background: Propranolol (PPL) has been suggested as an option for the treatment of various types of cancer. However, data regarding its effectiveness against oral cancer are scarce. Thus, we aimed to evaluate the antitumor potential of PPL in oral squamous cell carcinoma (OSCC) in vitro. Methods: OSCC cell lines, SCC-9, SCC-25, and Cal27, were treated with PPL at different times and concentrations. OSCC cells were treated with PPL alone or in combination with cisplatin (CDDP) or 5-fluorouracil (5-FU). Cell viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression of phosphorylated (p)-Akt, p-S6, p-PTEN, p-P65, and VEGF was verified by immunofluorescence. The migratory activity of OSCC cells was evaluated using a wound-healing assay. Results: PPL reduced OSCC cell viability in a dose- and time-dependent manner. Concentrations above 300 µM, 110 µM, and 100 µM for SCC-9, Cal27, and SCC-25, respectively, significantly eliminated tumor cells. The combination of PPL with CDDP and 5-FU enhanced their antitumor effects. There was a modest difference between the use of the IC30 and IC50 of PPL in the combinatory options. PPL downregulated p-P65 NF-ĸB and VEGF expression in SCC-9 and Cal27 cells but not in SCC-25 cells. PPL inhibited the phosphorylation of Akt and s6 and increased the phosphorylation of PTEN in all OSCC cell lines studied. PPL inhibited OSCC cell migration after 24 h of treatment. Conclusion: PPL was effective against oral cancer cells and enhanced standard-of-care. PPL inhibited cell viability and the expression of pAkt, NF-ĸB, and VEGF.
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spelling Propranolol inhibits cell viability and expression of the pro-tumorigenic proteins Akt, NF-ĸB, and VEGF in oral squamous cell carcinomabeta-adrenergic receptorBeta-blockersDistresshead and neck cancerHead and neck squamous cell carcinomaNF-kBNorepinephrineoral canceroral neoplasmsoral squamous cell carcinomaPropranololBackground: Propranolol (PPL) has been suggested as an option for the treatment of various types of cancer. However, data regarding its effectiveness against oral cancer are scarce. Thus, we aimed to evaluate the antitumor potential of PPL in oral squamous cell carcinoma (OSCC) in vitro. Methods: OSCC cell lines, SCC-9, SCC-25, and Cal27, were treated with PPL at different times and concentrations. OSCC cells were treated with PPL alone or in combination with cisplatin (CDDP) or 5-fluorouracil (5-FU). Cell viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression of phosphorylated (p)-Akt, p-S6, p-PTEN, p-P65, and VEGF was verified by immunofluorescence. The migratory activity of OSCC cells was evaluated using a wound-healing assay. Results: PPL reduced OSCC cell viability in a dose- and time-dependent manner. Concentrations above 300 µM, 110 µM, and 100 µM for SCC-9, Cal27, and SCC-25, respectively, significantly eliminated tumor cells. The combination of PPL with CDDP and 5-FU enhanced their antitumor effects. There was a modest difference between the use of the IC30 and IC50 of PPL in the combinatory options. PPL downregulated p-P65 NF-ĸB and VEGF expression in SCC-9 and Cal27 cells but not in SCC-25 cells. PPL inhibited the phosphorylation of Akt and s6 and increased the phosphorylation of PTEN in all OSCC cell lines studied. PPL inhibited OSCC cell migration after 24 h of treatment. Conclusion: PPL was effective against oral cancer cells and enhanced standard-of-care. PPL inhibited cell viability and the expression of pAkt, NF-ĸB, and VEGF.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Laboratory of Immunopharmacology Department of Basic Sciences School of Dentistry São Paulo State University (Unesp), São PauloDepartment of Diagnosis and Surgery School of Dentistry São Paulo State University (Unesp), São PauloPsychoneuroimmunology Laboratory Psychosomatic Research Center Oral Oncology Center School of Dentistry São Paulo State University (Unesp), São PauloLaboratory of Immunopharmacology Department of Basic Sciences School of Dentistry São Paulo State University (Unesp), São PauloDepartment of Diagnosis and Surgery School of Dentistry São Paulo State University (Unesp), São PauloPsychoneuroimmunology Laboratory Psychosomatic Research Center Oral Oncology Center School of Dentistry São Paulo State University (Unesp), São PauloFAPESP: # 2016/03965-2FAPESP: # 2017/18650-2FAPESP: #2016/00051-2FAPESP: #2016/24685-3FAPESP: #2016/25255-0Universidade Estadual Paulista (UNESP)Shibuya, Caroline Miho [UNESP]Tjioe, Kellen Cristine [UNESP]Oliveira, Sandra Helena Penha [UNESP]Bernabé, Daniel Galera [UNESP]2022-04-29T08:40:14Z2022-04-29T08:40:14Z2022-04-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://dx.doi.org/10.1016/j.archoralbio.2022.105383Archives of Oral Biology, v. 136.1879-15060003-9969http://hdl.handle.net/11449/23047910.1016/j.archoralbio.2022.1053832-s2.0-85125493670Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengArchives of Oral Biologyinfo:eu-repo/semantics/openAccess2024-04-11T20:16:33Zoai:repositorio.unesp.br:11449/230479Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-04-11T20:16:33Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Propranolol inhibits cell viability and expression of the pro-tumorigenic proteins Akt, NF-ĸB, and VEGF in oral squamous cell carcinoma
title Propranolol inhibits cell viability and expression of the pro-tumorigenic proteins Akt, NF-ĸB, and VEGF in oral squamous cell carcinoma
spellingShingle Propranolol inhibits cell viability and expression of the pro-tumorigenic proteins Akt, NF-ĸB, and VEGF in oral squamous cell carcinoma
Shibuya, Caroline Miho [UNESP]
beta-adrenergic receptor
Beta-blockers
Distress
head and neck cancer
Head and neck squamous cell carcinoma
NF-kB
Norepinephrine
oral cancer
oral neoplasms
oral squamous cell carcinoma
Propranolol
title_short Propranolol inhibits cell viability and expression of the pro-tumorigenic proteins Akt, NF-ĸB, and VEGF in oral squamous cell carcinoma
title_full Propranolol inhibits cell viability and expression of the pro-tumorigenic proteins Akt, NF-ĸB, and VEGF in oral squamous cell carcinoma
title_fullStr Propranolol inhibits cell viability and expression of the pro-tumorigenic proteins Akt, NF-ĸB, and VEGF in oral squamous cell carcinoma
title_full_unstemmed Propranolol inhibits cell viability and expression of the pro-tumorigenic proteins Akt, NF-ĸB, and VEGF in oral squamous cell carcinoma
title_sort Propranolol inhibits cell viability and expression of the pro-tumorigenic proteins Akt, NF-ĸB, and VEGF in oral squamous cell carcinoma
author Shibuya, Caroline Miho [UNESP]
author_facet Shibuya, Caroline Miho [UNESP]
Tjioe, Kellen Cristine [UNESP]
Oliveira, Sandra Helena Penha [UNESP]
Bernabé, Daniel Galera [UNESP]
author_role author
author2 Tjioe, Kellen Cristine [UNESP]
Oliveira, Sandra Helena Penha [UNESP]
Bernabé, Daniel Galera [UNESP]
author2_role author
author
author
dc.contributor.none.fl_str_mv Universidade Estadual Paulista (UNESP)
dc.contributor.author.fl_str_mv Shibuya, Caroline Miho [UNESP]
Tjioe, Kellen Cristine [UNESP]
Oliveira, Sandra Helena Penha [UNESP]
Bernabé, Daniel Galera [UNESP]
dc.subject.por.fl_str_mv beta-adrenergic receptor
Beta-blockers
Distress
head and neck cancer
Head and neck squamous cell carcinoma
NF-kB
Norepinephrine
oral cancer
oral neoplasms
oral squamous cell carcinoma
Propranolol
topic beta-adrenergic receptor
Beta-blockers
Distress
head and neck cancer
Head and neck squamous cell carcinoma
NF-kB
Norepinephrine
oral cancer
oral neoplasms
oral squamous cell carcinoma
Propranolol
description Background: Propranolol (PPL) has been suggested as an option for the treatment of various types of cancer. However, data regarding its effectiveness against oral cancer are scarce. Thus, we aimed to evaluate the antitumor potential of PPL in oral squamous cell carcinoma (OSCC) in vitro. Methods: OSCC cell lines, SCC-9, SCC-25, and Cal27, were treated with PPL at different times and concentrations. OSCC cells were treated with PPL alone or in combination with cisplatin (CDDP) or 5-fluorouracil (5-FU). Cell viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression of phosphorylated (p)-Akt, p-S6, p-PTEN, p-P65, and VEGF was verified by immunofluorescence. The migratory activity of OSCC cells was evaluated using a wound-healing assay. Results: PPL reduced OSCC cell viability in a dose- and time-dependent manner. Concentrations above 300 µM, 110 µM, and 100 µM for SCC-9, Cal27, and SCC-25, respectively, significantly eliminated tumor cells. The combination of PPL with CDDP and 5-FU enhanced their antitumor effects. There was a modest difference between the use of the IC30 and IC50 of PPL in the combinatory options. PPL downregulated p-P65 NF-ĸB and VEGF expression in SCC-9 and Cal27 cells but not in SCC-25 cells. PPL inhibited the phosphorylation of Akt and s6 and increased the phosphorylation of PTEN in all OSCC cell lines studied. PPL inhibited OSCC cell migration after 24 h of treatment. Conclusion: PPL was effective against oral cancer cells and enhanced standard-of-care. PPL inhibited cell viability and the expression of pAkt, NF-ĸB, and VEGF.
publishDate 2022
dc.date.none.fl_str_mv 2022-04-29T08:40:14Z
2022-04-29T08:40:14Z
2022-04-01
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.1016/j.archoralbio.2022.105383
Archives of Oral Biology, v. 136.
1879-1506
0003-9969
http://hdl.handle.net/11449/230479
10.1016/j.archoralbio.2022.105383
2-s2.0-85125493670
url http://dx.doi.org/10.1016/j.archoralbio.2022.105383
http://hdl.handle.net/11449/230479
identifier_str_mv Archives of Oral Biology, v. 136.
1879-1506
0003-9969
10.1016/j.archoralbio.2022.105383
2-s2.0-85125493670
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Archives of Oral Biology
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.source.none.fl_str_mv Scopus
reponame:Repositório Institucional da UNESP
instname:Universidade Estadual Paulista (UNESP)
instacron:UNESP
instname_str Universidade Estadual Paulista (UNESP)
instacron_str UNESP
institution UNESP
reponame_str Repositório Institucional da UNESP
collection Repositório Institucional da UNESP
repository.name.fl_str_mv Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)
repository.mail.fl_str_mv
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