Ocoxin Oral Solution Triggers DNA Damage and Cell Death in Ovarian Cancer
Ovarian cancer is the most fatal of all the reproductive cancers within the female population, mainly due to its late diagnosis that limits surgery and medical treatment. Classically, ovarian cancer therapy has included conventional chemotherapy, and other therapeutic approaches are now being used t...
| Autores: | , , , |
|---|---|
| Formato: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2024 |
| País: | España |
| Recursos: | Consejo Superior de Investigaciones Científicas (CSIC) |
| Repositorio: | DIGITAL.CSIC. Repositorio Institucional del CSIC |
| OAI Identifier: | oai:digital.csic.es:10261/381449 |
| Acesso em linha: | http://hdl.handle.net/10261/381449 |
| Access Level: | acceso abierto |
| Palavra-chave: | Ovarian cancer OOS Antioxidants DNA damage Cell death |
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Ocoxin Oral Solution Triggers DNA Damage and Cell Death in Ovarian CancerAlmaraz Postigo, SheilaSanz, EduardoPandiella, AtanasioDíaz-Rodríguez, ElenaOvarian cancerOOSAntioxidantsDNA damageCell deathOvarian cancer is the most fatal of all the reproductive cancers within the female population, mainly due to its late diagnosis that limits surgery and medical treatment. Classically, ovarian cancer therapy has included conventional chemotherapy, and other therapeutic approaches are now being used to treat these patients, but the outcomes of the disease are still poor. Therefore, new strategies are needed to improve life expectancy and life quality of ovarian cancer patients. Considering that, we investigated the effect of the nutritional supplement Ocoxin Oral Solution (OOS) in ovarian cancer models. OOS contains several nutritional supplements, some of them with demonstrated antitumoral action. In vitro studies showed that OOS inhibited the proliferation of several ovarian cancer cell lines, especially of those representative of the endometrioid subtype, in a time- and dose-dependent manner. A fast cell death induction after OOS treatment was observed, and when the molecular mechanisms leading to this effect were investigated, an activation of the DNA damage checkpoint was detected, as shown by activation (phosphorylation) of CHK1 and CHK2 kinases that was followed by the phosphorylation of the target protein histone H2AX. When tested in animal models of ovarian cancer, OOS reduced tumor growth without any observed secondary effects. Moreover, such reduction in tumor proliferation was caused by the induction of DNA damage as corroborated by the in vivo phosphorylation of CHK2 and Histone H2AX. Finally, OOS potentiated the action of carboplatin or olaparib, the standard of care treatments used in ovarian clinics, opening the possibility of including OOS in combination with those standard of care agents in patients with ovarian cancer.This work was partially supported by the Ministry of Economy and Competitiveness of Spain (BFU2015-71371-R and PID2020-115605RB-I00), the Instituto de Salud Carlos III through CIBERONC (CB16/12/00317), Junta de Castilla y León (CSI146P20), ALMOM, ACMUMA, UCCTA, the CRIS Cancer Foundation, Catalysis S.L. (Madrid, Spain) and the Regional Development Funding Program (FEDER) “A way to make Europe”.Peer reviewedMultidisciplinary Digital Publishing InstituteMinisterio de Economía y Competitividad (España)Ministerio de Ciencia, Innovación y Universidades (España)Agencia Estatal de Investigación (España)Instituto de Salud Carlos IIIJunta de Castilla y LeónFundación CRIS contra el CáncerEuropean CommissionConsejo Superior de Investigaciones Científicas [https://ror.org/02gfc7t72]202520252024info:eu-repo/semantics/articlehttp://purl.org/coar/resource_type/c_6501Publisher's versioninfo:eu-repo/semantics/publishedVersionapplication/pdfhttp://hdl.handle.net/10261/381449reponame:DIGITAL.CSIC. Repositorio Institucional del CSICinstname:Consejo Superior de Investigaciones Científicas (CSIC)Inglés#PLACEHOLDER_PARENT_METADATA_VALUE##PLACEHOLDER_PARENT_METADATA_VALUE#info:eu-repo/grantAgreement/MINECO//BFU2015-71371-Rinfo:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/PID2020-115605RB-I00The underlying dataset has been published as supplementary material of the article in the publisher platform at DOI https://doi.org/10.3390/nu16152416https://doi.org/10.3390/nu16152416Síinfo:eu-repo/semantics/openAccessoai:digital.csic.es:10261/3814492026-05-22T06:33:51Z |
| dc.title.none.fl_str_mv |
Ocoxin Oral Solution Triggers DNA Damage and Cell Death in Ovarian Cancer |
| title |
Ocoxin Oral Solution Triggers DNA Damage and Cell Death in Ovarian Cancer |
| spellingShingle |
Ocoxin Oral Solution Triggers DNA Damage and Cell Death in Ovarian Cancer Almaraz Postigo, Sheila Ovarian cancer OOS Antioxidants DNA damage Cell death |
| title_short |
Ocoxin Oral Solution Triggers DNA Damage and Cell Death in Ovarian Cancer |
| title_full |
Ocoxin Oral Solution Triggers DNA Damage and Cell Death in Ovarian Cancer |
| title_fullStr |
Ocoxin Oral Solution Triggers DNA Damage and Cell Death in Ovarian Cancer |
| title_full_unstemmed |
Ocoxin Oral Solution Triggers DNA Damage and Cell Death in Ovarian Cancer |
| title_sort |
Ocoxin Oral Solution Triggers DNA Damage and Cell Death in Ovarian Cancer |
| dc.creator.none.fl_str_mv |
Almaraz Postigo, Sheila Sanz, Eduardo Pandiella, Atanasio Díaz-Rodríguez, Elena |
| author |
Almaraz Postigo, Sheila |
| author_facet |
Almaraz Postigo, Sheila Sanz, Eduardo Pandiella, Atanasio Díaz-Rodríguez, Elena |
| author_role |
author |
| author2 |
Sanz, Eduardo Pandiella, Atanasio Díaz-Rodríguez, Elena |
| author2_role |
author author author |
| dc.contributor.none.fl_str_mv |
Ministerio de Economía y Competitividad (España) Ministerio de Ciencia, Innovación y Universidades (España) Agencia Estatal de Investigación (España) Instituto de Salud Carlos III Junta de Castilla y León Fundación CRIS contra el Cáncer European Commission Consejo Superior de Investigaciones Científicas [https://ror.org/02gfc7t72] |
| dc.subject.none.fl_str_mv |
Ovarian cancer OOS Antioxidants DNA damage Cell death |
| topic |
Ovarian cancer OOS Antioxidants DNA damage Cell death |
| description |
Ovarian cancer is the most fatal of all the reproductive cancers within the female population, mainly due to its late diagnosis that limits surgery and medical treatment. Classically, ovarian cancer therapy has included conventional chemotherapy, and other therapeutic approaches are now being used to treat these patients, but the outcomes of the disease are still poor. Therefore, new strategies are needed to improve life expectancy and life quality of ovarian cancer patients. Considering that, we investigated the effect of the nutritional supplement Ocoxin Oral Solution (OOS) in ovarian cancer models. OOS contains several nutritional supplements, some of them with demonstrated antitumoral action. In vitro studies showed that OOS inhibited the proliferation of several ovarian cancer cell lines, especially of those representative of the endometrioid subtype, in a time- and dose-dependent manner. A fast cell death induction after OOS treatment was observed, and when the molecular mechanisms leading to this effect were investigated, an activation of the DNA damage checkpoint was detected, as shown by activation (phosphorylation) of CHK1 and CHK2 kinases that was followed by the phosphorylation of the target protein histone H2AX. When tested in animal models of ovarian cancer, OOS reduced tumor growth without any observed secondary effects. Moreover, such reduction in tumor proliferation was caused by the induction of DNA damage as corroborated by the in vivo phosphorylation of CHK2 and Histone H2AX. Finally, OOS potentiated the action of carboplatin or olaparib, the standard of care treatments used in ovarian clinics, opening the possibility of including OOS in combination with those standard of care agents in patients with ovarian cancer. |
| publishDate |
2024 |
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2024 2025 2025 |
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info:eu-repo/semantics/article http://purl.org/coar/resource_type/c_6501 Publisher's version info:eu-repo/semantics/publishedVersion |
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article |
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publishedVersion |
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http://hdl.handle.net/10261/381449 |
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http://hdl.handle.net/10261/381449 |
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Inglés |
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Inglés |
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#PLACEHOLDER_PARENT_METADATA_VALUE# #PLACEHOLDER_PARENT_METADATA_VALUE# info:eu-repo/grantAgreement/MINECO//BFU2015-71371-R info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/PID2020-115605RB-I00 The underlying dataset has been published as supplementary material of the article in the publisher platform at DOI https://doi.org/10.3390/nu16152416 https://doi.org/10.3390/nu16152416 Sí |
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info:eu-repo/semantics/openAccess |
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application/pdf |
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Multidisciplinary Digital Publishing Institute |
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Multidisciplinary Digital Publishing Institute |
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reponame:DIGITAL.CSIC. Repositorio Institucional del CSIC instname:Consejo Superior de Investigaciones Científicas (CSIC) |
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Consejo Superior de Investigaciones Científicas (CSIC) |
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