Akt mediates TIGAR induction in HeLa cells following PFKFB3 inhibition.
FEBS Lett
; 590(17): 2915-26, 2016 09.
Article
en En
| MEDLINE
| ID: mdl-27491040
ABSTRACT
Neoplastic cells metabolize higher amounts of glucose relative to normal cells in order to cover increased energetic and anabolic needs. Inhibition of the glycolytic enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) diminishes cancer cell proliferation and tumour growth in animals. In this work, we investigate the crosstalk between PFKFB3 and TIGAR (TP53-Induced Glycolysis and Apoptosis Regulator), a protein known to protect cells from oxidative stress. Our results show consistent TIGAR induction in HeLa cells in response to PFKFB3 knockdown. Upon PFKFB3 silencing, cells undergo oxidative stress and trigger Akt phosphorylation. This leads to induction of a TIGAR-mediated prosurvival pathway that reduces both oxidative stress and cell death. As TIGAR is known to have a role in DNA repair, it could serve as a potential target for the development of effective antineoplastic therapies.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Estrés Oxidativo
/
Fosfofructoquinasa-2
/
Péptidos y Proteínas de Señalización Intracelular
/
Neoplasias
Límite:
Humans
Idioma:
En
Revista:
FEBS Lett
Año:
2016
Tipo del documento:
Article
País de afiliación:
España