LncRNA SNHG3 induces EMT and sorafenib resistance by modulating the miR-128/CD151 pathway in hepatocellular carcinoma
LncRNA SNHG3 induces EMT and sorafenib resistance by modulating the miR-128/CD151 pathway in hepatocellular carcinoma
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LncRNA SNHG3 通过调节肝细胞癌中的 miR-128/CD151 通路诱导 EMT 和索拉非尼耐药。
DOI：
10.1002/jcp.27095
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发表时间：
2019-03-01
影响因子：
5.6
通讯作者：
Ke, Ai-Wu
中科院分区：
文献类型：
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作者：
Zhang, Peng-Fei;Wang, Fei;Ke, Ai-Wu
长链非编码rna （lncRNAs）的失调在包括肝细胞癌（HCC）在内的癌变和肿瘤进展中起着重要作用。小核仁RNA宿主基因3 （SNHG3）被认为是与HCC患者预后不良相关的lncRNA。在这里，我们报道了SNHG3在高转移性HCC （HCCLM3）细胞中的表达明显高于低转移性HCC细胞（Hep3B和PLC/PRF/5）。此外，SNHG3的强制表达促进了HCC中的细胞侵袭、上皮-间质转化（EMT）和索拉非尼耐药。此外，SNHG3过表达通过miR-128/CD151级联激活诱导HCC细胞EMT。临床上，我们的数据显示SNHG3表达增加与HCC生存结局和索拉非尼应答不良相关。这些数据表明，SNHG3可能是一种新的治疗靶点和预测索拉非尼治疗HCC反应的生物标志物。
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.