Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/113060
Título: Apoptosis pathways triggered by a potent antiproliferative hybrid chalcone on human melanoma cells
Autores/as: Rodríguez, Irene
Saavedra Díaz, Ester Gloria 
Del Rosario, Henoc 
Perdomo Díaz, Juan 
Quintana Aguiar, José Martín 
Prencipe, Filippo
Oliva, Paola
Romagnoli, Romeo
Estévez, Francisco 
Palabras clave: Apoptosis
Caspases
Cytotoxicity
Extracellular Signal-Regulated Kinases
Hybrid Chalcones, et al.
Fecha de publicación: 2021
Publicación seriada: International Journal of Molecular Sciences 
Resumen: The World Health Organization reported that approximately 324,000 new cases of melanoma skin cancer were diagnosed worldwide in 2020. The incidence of melanoma has been increasing over the past decades. Targeting apoptotic pathways is a potential therapeutic strategy in the transition to preclinical models and clinical trials. Some naturally occurring products and synthetic derivatives are apoptosis inducers and may represent a realistic option in the fight against the disease. Thus, chalcones have received considerable attention due to their potential cytotoxicity against cancer cells. We have previously reported a chalcone containing an indole and a pyridine heterocyclic rings and an α-bromoacryloylamido radical which displays potent antiproliferative activity against several tumor cell lines. In this study, we report that this chalcone is a potent apoptotic inducer for human melanoma cell lines SK-MEL-1 and MEL-HO. Cell death was associated with mitochon-drial cytochrome c release and poly(ADP-ribose) polymerase cleavage and was prevented by a non-specific caspase inhibitor. Using SK-MEL-1 as a model, we found that the mechanism of cell death involves (i) the generation of reactive oxygen species, (ii) activation of the extrinsic and intrinsic apoptotic and mitogen-activated protein kinase pathways, (iii) upregulation of TRAIL, DR4 and DR5, (iv) downregulation of p21Cip1/WAF1 and, inhibition of the NF-κB pathway.
URI: http://hdl.handle.net/10553/113060
ISSN: 1661-6596
DOI: 10.3390/ijms222413462
Fuente: International Journal of Molecular Sciences [ISSN 1661-6596], v. 22 (24), 13462, (Diciembre 2021)
Colección:Artículos
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