Galectin 1 induces hepatocellular carcinoma EMT and sorafenib resistance by activating FAK/PI3K/AKT signaling
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 avb3 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.
Cell Death and Disease