Ethanol Enhances Hyperthermia-Induced Cell Death in Human Leukemia Cells
Ethanol has been shown to exhibit therapeutic properties as an ablative agent alone and in combination with thermal ablation. Ethanol may also increase sensitivity of cancer cells to certain physical and chemical antitumoral agents. The aim of our study was to assess the potential influence of nonto...
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| Published in | International journal of molecular sciences Vol. 22; no. 9; p. 4948 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
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MDPI AG
06.05.2021
MDPI |
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| Online Access | Get full text |
| ISSN | 1422-0067 1661-6596 1422-0067 |
| DOI | 10.3390/ijms22094948 |
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| Abstract | Ethanol has been shown to exhibit therapeutic properties as an ablative agent alone and in combination with thermal ablation. Ethanol may also increase sensitivity of cancer cells to certain physical and chemical antitumoral agents. The aim of our study was to assess the potential influence of nontoxic concentrations of ethanol on hyperthermia therapy, an antitumoral modality that is continuously growing and that can be combined with classical chemotherapy and radiotherapy to improve their efficiency. Human leukemia cells were included as a model in the study. The results indicated that ethanol augments the cytotoxicity of hyperthermia against U937 and HL60 cells. The therapeutic benefit of the hyperthermia/ethanol combination was associated with an increase in the percentage of apoptotic cells and activation of caspases-3, -8 and -9. Apoptosis triggered either by hyperthermia or hyperthermia/ethanol was almost completely abolished by a caspase-8 specific inhibitor, indicating that this caspase plays a main role in both conditions. The role of caspase-9 in hyperthermia treated cells acquired significance whether ethanol was present during hyperthermia since the alcohol enhanced Bid cleavage, translocation of Bax from cytosol to mitochondria, release of mitochondrial apoptogenic factors, and decreased of the levels of the anti-apoptotic factor myeloid cell leukemia-1 (Mcl-1). The enhancement effect of ethanol on hyperthermia-activated cell death was associated with a reduction in the expression of HSP70, a protein known to interfere in the activation of apoptosis at different stages. Collectively, our findings suggest that ethanol could be useful as an adjuvant in hyperthermia therapy for cancer. |
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| AbstractList | Ethanol has been shown to exhibit therapeutic properties as an ablative agent alone and in combination with thermal ablation. Ethanol may also increase sensitivity of cancer cells to certain physical and chemical antitumoral agents. The aim of our study was to assess the potential influence of nontoxic concentrations of ethanol on hyperthermia therapy, an antitumoral modality that is continuously growing and that can be combined with classical chemotherapy and radiotherapy to improve their efficiency. Human leukemia cells were included as a model in the study. The results indicated that ethanol augments the cytotoxicity of hyperthermia against U937 and HL60 cells. The therapeutic benefit of the hyperthermia/ethanol combination was associated with an increase in the percentage of apoptotic cells and activation of caspases-3, -8 and -9. Apoptosis triggered either by hyperthermia or hyperthermia/ethanol was almost completely abolished by a caspase-8 specific inhibitor, indicating that this caspase plays a main role in both conditions. The role of caspase-9 in hyperthermia treated cells acquired significance whether ethanol was present during hyperthermia since the alcohol enhanced Bid cleavage, translocation of Bax from cytosol to mitochondria, release of mitochondrial apoptogenic factors, and decreased of the levels of the anti-apoptotic factor myeloid cell leukemia-1 (Mcl-1). The enhancement effect of ethanol on hyperthermia-activated cell death was associated with a reduction in the expression of HSP70, a protein known to interfere in the activation of apoptosis at different stages. Collectively, our findings suggest that ethanol could be useful as an adjuvant in hyperthermia therapy for cancer. Ethanol has been shown to exhibit therapeutic properties as an ablative agent alone and in combination with thermal ablation. Ethanol may also increase sensitivity of cancer cells to certain physical and chemical antitumoral agents. The aim of our study was to assess the potential influence of nontoxic concentrations of ethanol on hyperthermia therapy, an antitumoral modality that is continuously growing and that can be combined with classical chemotherapy and radiotherapy to improve their efficiency. Human leukemia cells were included as a model in the study. The results indicated that ethanol augments the cytotoxicity of hyperthermia against U937 and HL60 cells. The therapeutic benefit of the hyperthermia/ethanol combination was associated with an increase in the percentage of apoptotic cells and activation of caspases-3, -8 and -9. Apoptosis triggered either by hyperthermia or hyperthermia/ethanol was almost completely abolished by a caspase-8 specific inhibitor, indicating that this caspase plays a main role in both conditions. The role of caspase-9 in hyperthermia treated cells acquired significance whether ethanol was present during hyperthermia since the alcohol enhanced Bid cleavage, translocation of Bax from cytosol to mitochondria, release of mitochondrial apoptogenic factors, and decreased of the levels of the anti-apoptotic factor myeloid cell leukemia-1 (Mcl-1). The enhancement effect of ethanol on hyperthermia-activated cell death was associated with a reduction in the expression of HSP70, a protein known to interfere in the activation of apoptosis at different stages. Collectively, our findings suggest that ethanol could be useful as an adjuvant in hyperthermia therapy for cancer.Ethanol has been shown to exhibit therapeutic properties as an ablative agent alone and in combination with thermal ablation. Ethanol may also increase sensitivity of cancer cells to certain physical and chemical antitumoral agents. The aim of our study was to assess the potential influence of nontoxic concentrations of ethanol on hyperthermia therapy, an antitumoral modality that is continuously growing and that can be combined with classical chemotherapy and radiotherapy to improve their efficiency. Human leukemia cells were included as a model in the study. The results indicated that ethanol augments the cytotoxicity of hyperthermia against U937 and HL60 cells. The therapeutic benefit of the hyperthermia/ethanol combination was associated with an increase in the percentage of apoptotic cells and activation of caspases-3, -8 and -9. Apoptosis triggered either by hyperthermia or hyperthermia/ethanol was almost completely abolished by a caspase-8 specific inhibitor, indicating that this caspase plays a main role in both conditions. The role of caspase-9 in hyperthermia treated cells acquired significance whether ethanol was present during hyperthermia since the alcohol enhanced Bid cleavage, translocation of Bax from cytosol to mitochondria, release of mitochondrial apoptogenic factors, and decreased of the levels of the anti-apoptotic factor myeloid cell leukemia-1 (Mcl-1). The enhancement effect of ethanol on hyperthermia-activated cell death was associated with a reduction in the expression of HSP70, a protein known to interfere in the activation of apoptosis at different stages. Collectively, our findings suggest that ethanol could be useful as an adjuvant in hyperthermia therapy for cancer. |
| Author | Hernández, Inmaculada Quintana, Mercedes Saavedra, Ester Estévez, Francisco Quintana, José González, Ignacio del Rosario, Henoc |
| AuthorAffiliation | Departamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología, Instituto Universitario de Investigaciones Biomédicas y Sanitarias (IUIBS), Universidad de Las Palmas de Gran Canaria, 35016 Las Palmas de Gran Canaria, Spain; mercedes.quintana101@alu.ulpgc.es (M.Q.); ester.saavedra102@alu.ulpgc.es (E.S.); henoc.del101@alu.ulpgc.es (H.d.R.); ignacio.gonzalez@ulpgc.es (I.G.); servanda.hernandez@ulpgc.es (I.H.); francisco.estevez@ulpgc.es (F.E.) |
| AuthorAffiliation_xml | – name: Departamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología, Instituto Universitario de Investigaciones Biomédicas y Sanitarias (IUIBS), Universidad de Las Palmas de Gran Canaria, 35016 Las Palmas de Gran Canaria, Spain; mercedes.quintana101@alu.ulpgc.es (M.Q.); ester.saavedra102@alu.ulpgc.es (E.S.); henoc.del101@alu.ulpgc.es (H.d.R.); ignacio.gonzalez@ulpgc.es (I.G.); servanda.hernandez@ulpgc.es (I.H.); francisco.estevez@ulpgc.es (F.E.) |
| Author_xml | – sequence: 1 givenname: Mercedes surname: Quintana fullname: Quintana, Mercedes – sequence: 2 givenname: Ester orcidid: 0000-0002-1717-386X surname: Saavedra fullname: Saavedra, Ester – sequence: 3 givenname: Henoc surname: del Rosario fullname: del Rosario, Henoc – sequence: 4 givenname: Ignacio surname: González fullname: González, Ignacio – sequence: 5 givenname: Inmaculada surname: Hernández fullname: Hernández, Inmaculada – sequence: 6 givenname: Francisco orcidid: 0000-0002-9728-2774 surname: Estévez fullname: Estévez, Francisco – sequence: 7 givenname: José orcidid: 0000-0001-8225-4538 surname: Quintana fullname: Quintana, José |
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| CitedBy_id | crossref_primary_10_1016_j_isci_2024_111298 crossref_primary_10_1007_s11033_022_07705_6 crossref_primary_10_3390_curroncol30060399 crossref_primary_10_3390_polym13234259 crossref_primary_10_1002_tox_24080 crossref_primary_10_1016_j_procbio_2022_07_001 |
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| SubjectTerms | Apoptosis Cancer therapies Cell cycle Cell death Chemotherapy Cytochrome Ethanol Fever Flow cytometry Hyperthermia Leukemia Radiation therapy |
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| Title | Ethanol Enhances Hyperthermia-Induced Cell Death in Human Leukemia Cells |
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