IFN-α-2b induces apoptosis by decreasing cellular cholesterol levels in rat preneoplastic hepatocytes
; Vera, Marina Cecilia
; Ferretti, Anabela
; Lucci, Alvaro
; Comanzo, Carla Gabriela
; Lambertucci, Flavia
; Ceballos Mancini, María Paula
; Carrillo, Maria Cristina 
Otros responsables
Fecha
09/2020
Editorial
Academic Press Ltd - Elsevier Science Ltd
Revista
Cytokine
Título del libro
Nombre del evento
Fecha del evento
Institución organizadora
ISSN
1043-4666
eISSN
ISBN
Idioma
Inglés
Tipo del evento
Clasificación temática
Palabras clave
Resumen
IFN-α administration to patients has been long discouraged and pushed back by new and apparently better drugs; however the adverse secondary effect, the high costs and the lack of specific action, make these new drugs hard to be used and put IFN-α again in the eye of the researchers. IFN-α-2b was demonstrated to induce apoptosis and modulation of lipid metabolism and the mechanisms are still unknown. Here, we sought to find the link between these features using a model of early stage cancer development. Using in vitro and in vivo approaches, we evaluated apoptosis and lipid metabolism. IFN-α-2b induced changes in hepatic cholesterol mass due to decreased synthesis and increased secretion. Interestingly, the drop in cellular cholesterol levels was necessary for IFN-α-2b to induce apoptosis. Results presented in this paper show the complexity of the action of IFN-α-2b on the early stages of liver cancer development. We show for the first time an interrelationship between cholesterol, apoptosis and IFN-α-2b. This makes clear the need for a reevaluation of IFN-α-2b action in order to develop softer, safer and more bearable derivatives. In this regard, knowing the molecular mechanisms by which IFN-α exerts its cellular actions is of crucial importance, and it is the main condition for therapy success for classical and new malignancies.
Colecciones
Aprobación
Revisión
Complementado por
Referenciado por
Licencia Creative Commons
Excepto donde se indique lo contrario, la licencia de este ítem se describe como by-nc-sa
