Galectin-1 induces hepatocellular carcinoma EMT and sorafenib resistance by activating FAK/PI3K/AKT signaling.
Cell Death Dis
; 7: e2201, 2016 Apr 21.
Article
en En
| MEDLINE
| ID: mdl-27100895
ABSTRACT
Galectin-1 (Gal-1) is involved in several pathological activities associated with tumor progression and chemoresistance, however, the role and molecular mechanism of Gal-1 activity in hepatocellular carcinoma (HCC) epithelial-mesenchymal transition (EMT) and sorafenib resistance remain enigmatic. In the present study, forced Gal-1 expression promoted HCC progression and sorafenib resistance. Gal-1 elevated αvß3-integrin expression, leading to AKT activation. Moreover, Gal-1 overexpression induced HCC cell EMT via PI3K/AKT cascade activation. Clinically, our data revealed that Gal-1 overexpression is correlated with poor HCC survival outcomes and sorafenib response. These data suggest that Gal-1 may be a potential therapeutic target for HCC and a biomarker for predicting response to sorafenib treatment.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Compuestos de Fenilurea
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Niacinamida
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Fosfatidilinositol 3-Quinasas
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Galectina 1
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Proteínas Proto-Oncogénicas c-akt
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Quinasa 1 de Adhesión Focal
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Transición Epitelial-Mesenquimal
Tipo de estudio:
Prognostic_studies
Idioma:
En
Revista:
Cell Death Dis
Año:
2016
Tipo del documento:
Article
País de afiliación:
China