2023, Número 2
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Odovtos-Int J Dent Sc 2023; 25 (2)
Efecto anticancerígeno relacionado con el autofago del extracto de uva y el extracto de tomate: estudio ex vivo
Elshafei MM, Helmy IM, Sayed MM, Farag DB, Shebl IM, Ghazy ES, Afifi NS
Idioma: Ingles.
Referencias bibliográficas: 56
Paginas: 78-92
Archivo PDF: 674.74 Kb.
RESUMEN
Las células se someten a autofagia para salvarse de lesiones, pero la autofagia progresiva puede provocar la muerte celular. Este estudio caracterizó y comparó el efecto de los extractos de uva (resveratrol) y tomate (licopeno) y su combinación en la modulación de miARN relacionado con la autofagia y su gen diana en la línea celular de carcinoma de células escamosas. Se realizó análisis de acoplamiento para extractos y genes seleccionados. Se utilizaron ensayos de metil tiazol tetrazolio para evaluar la citotoxicidad de los extractos y su combinación frente a las células HEp-2. qRT-PCR se utilizó para cuantificar los cambios en la expresión génica. Los datos fueron analizados estadísticamente. El miARN-20a se identificó como un efector potencial en el cáncer de laringe y el secuenciasoma-1 (SQSTM1) fue su gen diana. El análisis de acoplamiento mostró que el resveratrol interactuaba con miRNA-20a y mostraba menos afinidad hacia SQSTM1. Se predijeron enlaces de hidrógeno e interacciones hidrofóbicas. Por el contrario, el licopeno mostró menos afinidad hacia el miARN-20a que el resveratrol. El aumento de las dosis de resveratrol, licopeno y su combinación indujo una reducción estadísticamente significativa en el porcentaje medio de viabilidad y los cambios medios en la expresión de miRNA-20a y SQSTM1 en las células HEp-2 tratadas. La correlación de Pearson mostró una correlación positiva estadísticamente significativa entre miRNA-20a y SQSTM1 (R=0,812, p≤0,001). Los extractos de uva y tomate y su combinación muestran una citotoxicidad prometedora contra las células HEp-2 de forma dependiente de la dosis y el tiempo. Ambos extractos reducen la expresión de miRNA-20a y SQSTM1 con la posterior inhibición de la autofagia y promoción de la apoptosis en células HEp-2.
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