Galectin-1 induces hepatocellular carcinoma EMT and sorafenib resistance by activating FAK/PI3K/AKT signaling

被引：192
|
作者：
Zhang, P-F [1 ]
Li, K-S [2 ]
Shen, Y-h [1 ]
Gao, P-T [1 ]
Dong, Z-R [1 ]
Cai, J-B [1 ]
Zhang, C. [1 ]
Huang, X-Y [1 ]
Tian, M-X [1 ]
Hu, Z-Q [1 ]
Gao, D-M [1 ]
Fan, J. [1 ,3 ]
Ke, A-W [1 ]
Shi, G-M [1 ]
机构：
[1] Fudan Univ, Liver Canc Inst, Zhongshan Hosp, Key Lab Carcinogenesis & Canc Invas,Minist Educ, 180 Fenglin Rd, Shanghai 200032, Peoples R China
[2] Shanghai Jiao Tong Univ, Sch Med, Renji Hosp, State Key Lab Oncogenes & Related Genes,Shanghai, Shanghai 200032, Peoples R China
[3] Fudan Univ, Inst Biomed Sci, Ctr Canc, Shanghai 200031, Peoples R China
来源：
CELL DEATH & DISEASE | 2016年 / 7卷
基金：
中国国家自然科学基金;
关键词：
EPITHELIAL-MESENCHYMAL TRANSITION; TUMOR-METASTASIS; CANCER; PROGRESSION; CELLS; OVEREXPRESSION; ALPHA-V-BETA-3; STEMNESS; THERAPY;
D O I：
10.1038/cddis.2015.324
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
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 alpha v beta 3-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.
引用
收藏
页码：e2201 / e2201
页数：9
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