Chalcone-induced apoptosis through caspase-dependent intrinsic pathways in human hepatocellular carcinoma cells
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Fecha
2016-02
Profesor/a Guía
Facultad/escuela
Idioma
en
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Título del volumen
Editor
MDPI AG
Nombre de Curso
Licencia CC
Atribution 4.0 International (CC BY 4.0)
Licencia CC
https://creativecommons.org/licenses/by/4.0/deed.es
Resumen
Hepatocellular carcinoma (HCC) is one of the most commonly diagnosed cancers
worldwide. Chemoprevention of HCC can be achieved through the use of natural or synthetic
compounds that reverse, suppress or prevent the development of cancer progression. In this
study, we investigated the antiproliferative effects and the mechanism of action of two compounds,
2,3,41
-trimethoxy-21
-hydroxy-chalcone (CH1) and 31
-bromo-3,4-dimethoxy-chalcone (CH2), over
human hepatoma cells (HepG2 and Huh-7) and cultured mouse hepatocytes (HepM). Cytotoxic
effects were observed over the HepG2 and Huh-7, and no effects were observed over the HepM.
For HepG2 cells, treated separately with each chalcone, typical apoptotic laddering and nuclear
condensation were observed. Additionally, the caspases and Bcl-2 family proteins activation by using
Western blotting and immunocytochemistry were studied. Caspase-8 was not activated, but caspase-3
and -9 were both activated by chalcones in HepG2 cells. Chalcones also induced reactive oxygen
species (ROS) accumulation after 4, 8 and 24 h of treatment in HepG2 cells. These results suggest
that apoptosis in HepG2 was induced through: (i) a caspase-dependent intrinsic pathway; and (ii) by
alterations in the cellular levels of Bcl-2 family proteins, and also, that the chalcone moiety could be
a potent candidate as novel anticancer agents acting on human hepatomas.
Notas
Indexación: Scopus.
Palabras clave
Chalcone, Caspase, Reactive Oxygen Species
Citación
International Journal of Molecular Sciences. Volume 17, Issue. 222 February 2016. Article number 260
DOI
10.3390/ijms17020260