Silencing of Glut1 induces chemoresistance via modulation of Akt/GSK-3ß/ß-catenin/survivin signaling pathway in breast cancer cells.
Arch Biochem Biophys
; 636: 110-122, 2017 12 15.
Article
en En
| MEDLINE
| ID: mdl-28803837
ABSTRACT
Cancer cells require increased aerobic glycolysis to support rapid cell proliferation. For their increased energy demands, cancer cells express glucose transporter (Glut) proteins at a high level. Glut1 is associated with basal-like breast cancer and is considered a potential therapeutic target. To investigate the possibility of Glut1 as a therapeutic target in breast cancer cells, we downregulated Glut1 in triple-negative breast cancer (TNBC) cell lines using a short hairpin system. We determined whether Glut1 silencing might enhance anti-proliferative effect of chemotherapeutic agents. Contrary to our hypothesis, ablation of Glut1 attenuated apoptosis and increased drug resistance via upregulation of p-Akt/p-GSK-3ß (Ser9)/ß-catenin/survivin. These results indicated that the potential of Glut1 as a therapeutic target should be carefully reevaluated.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Transducción de Señal
/
Regulación Neoplásica de la Expresión Génica
/
Regulación hacia Arriba
/
Resistencia a Antineoplásicos
/
Silenciador del Gen
/
Proteínas Proto-Oncogénicas c-akt
/
Proteínas Inhibidoras de la Apoptosis
/
Beta Catenina
/
Transportador de Glucosa de Tipo 1
/
Glucógeno Sintasa Quinasa 3 beta
Límite:
Female
/
Humans
Idioma:
En
Revista:
Arch Biochem Biophys
Año:
2017
Tipo del documento:
Article
País de afiliación:
Corea del Sur