Central role of cell cycle regulation in the antitumoral action of ocoxin

[EN]Nutritional supplements which include natural antitumoral compounds could represent safe and efficient additives for cancer patients. One such nutritional supplement, Ocoxin Oral solution (OOS), is a composite formulation that contains several antioxidants and exhibits antitumoral properties in...

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Detalles Bibliográficos
Autores: Pérez-Peña, Javier, Díaz Rodríguez, María Elena, Sanz, Eduardo, Pandiella Alonso, Atanasio
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2019
País:España
Institución:Universidad de Salamanca (USAL)
Repositorio:GREDOS. Repositorio Institucional de la Universidad de Salamanca
OAI Identifier:oai:dnet:gredos______::27b69dc6030b4ad9df78e77c3578e9e1
Acceso en línea:http://hdl.handle.net/10366/171371
Access Level:acceso embargado
Palabra clave:Acute myeloid leukemia
Antioxidants
Apoptosis
Cell cycle
p27
Small-cell lung cancer
Zinc Sulfate
Ascorbic Acid
Cell Cycle
Plant Extracts
Gene Expression Regulation
Humans
Vitamin B 6
Cell Line
Neoplasms
Transcriptome
Folic Acid
Pantothenic Acid
Vitamin B 12
Animals
Mice
24 Ciencias de la Vida
2302.21 Biología Molecular
neoplasias
ácido pantoténico
humanos
ratones
línea celular
vitamina B 6
extractos de plantas
ácido fólico
regulación de la expresión génica
animales
ácido ascórbico
ciclo celular
transcriptoma
vitamina B 12
sulfato de zinc
Descripción
Sumario:[EN]Nutritional supplements which include natural antitumoral compounds could represent safe and efficient additives for cancer patients. One such nutritional supplement, Ocoxin Oral solution (OOS), is a composite formulation that contains several antioxidants and exhibits antitumoral properties in several in vitro and in vivo tumor conditions. Here, we performed a functional genomic analysis to uncover the mechanism of the antitumoral action of OOS. Using in vivo models of acute myelogenous leukemia (AML, HEL cells, representative of a liquid tumor) and small-cell lung cancer (GLC-8, representative of a solid tumor), we showed that OOS treatment altered the transcriptome of xenografted tumors created by subcutaneously implanting these cells. Functional transcriptomic studies pointed to a cell cycle deregulation after OOS treatment. The main pathway responsible for this deregulation was the E2F-TFDP route, which was affected at different points. The alterations ultimately led to a decrease in pathway activation. Moreover, when OOS-deregulated genes in the AML context were analyzed in patient samples, a clear correlation with their levels and prognosis was observed. Together, these data led us to suggest that the antitumoral effect of OOS is due to blockade of cell cycle progression mainly caused by the action of OOS on the E2F-TFDP pathway.