LncRNA SNHG3 induces EMT and sorafenib resistance by modulating the miR-128/CD151 pathway in hepatocellular carcinoma

被引：190

作者：

Zhang, Peng-Fei ^{[1
,2
]}

Wang, Fei ^{[2
]}

Wu, Jing ^{[2
]}

Wu, Yin ^{[2
]}

Huang, Wei ^{[2
]}

Liu, Dong ^{[2
]}

Huang, Xiao-Yong ^{[1
]}

Zhang, Xue-Mei ^{[2
]}

Ke, Ai-Wu ^{[1
]}

机构：

[1] Fudan Univ, Zhongshan Hosp, Key Lab Carcinogenesis & Canc Invas, Liver Canc Inst,Minist Educ, Shanghai 200120, Peoples R China

[2] Tongji Univ, Sch Med, Dept Oncol, Shanghai East Hosp, Shanghai 200120, Peoples R China

来源：

JOURNAL OF CELLULAR PHYSIOLOGY | 2019年 / 234卷 / 03期

基金：

中国国家自然科学基金;

关键词：

epithelial-mesenchymal transition (EMT); hepatocellular carcinoma (HCC); small nucleolar RNA host gene 3 (SNHG3); sorafenib resistance; PROMOTES; METASTASIS; PROGNOSIS;

D O I：

10.1002/jcp.27095

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Dysregulation of long noncoding RNAs (lncRNAs) plays important roles in carcinogenesis and tumor progression, including hepatocellular carcinoma (HCC). Small nucleolar RNA host gene 3 (SNHG3) has been considered as an lncRNA to be associated with a poor prognosis in patients with HCC. Here, we reported that SNHG3 expression was significantly higher in the highly metastatic HCC (HCCLM3) cells compared with the lowly metastatic HCC cells (Hep3B and PLC/PRF/5). Furthermore, forced expression of SNHG3 promoted cell invasion, epithelial-mesenchymal transition (EMT), and sorafenib resistance in HCC. Moreover, SNHG3 overexpression induced HCC cells EMT via miR-128/CD151 cascade activation. Clinically, our data revealed that increased SNHG3 expression is correlated with poor HCC survival outcomes and sorafenib response. These data suggest that SNHG3 may be a novel therapeutic target and a biomarker for predicting response to sorafenib treatment of HCC.

引用

页码：2788 / 2794

页数：7

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