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首页> 外文期刊>Journal of cellular physiology. >Long noncoding RNASPRY4-IT1 promotes proliferation and metastasis of hepatocellular carcinoma via mediating TNF signaling pathway
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Long noncoding RNASPRY4-IT1 promotes proliferation and metastasis of hepatocellular carcinoma via mediating TNF signaling pathway

机译：长非编码RNASPRY4-IT1促进增殖和肝细胞癌的转移调节肿瘤坏死因子信号通路

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摘要

Our previous studies have indicated that long noncoding RNA (IncRNA) SPRY4 intronic transcript 1 (SPRY4-IT1) was highly expressed in hepatocellular carcinoma (HCC). However, it still remained unclear how SPRY4-IT1 worked in tumorgenesis in HCC. In this study, we tested the overexpression of SPRY4-IT1 in HCC tissues and cells through a quantitative real-time polymerase chain reaction. Statistical analyses showed that the upregulation had an association with the tumor node metastasis stage, thrombin time, and alkaline phosphatase. Furthermore, SPRY4-IT1 could be involved in cell proliferation, metastasis, and the epithelial-to-mesenchymal transition (EMT) process in HCC in vitro and in vivo. RNA-sequencing and transcriptome analysis were carried out to explore the mechanism of SPRY4-IT1 in HCC. With SPRY4-IT1 being knocked down or overexpressed, the level of proteins in the tumor necrosis factor (TNF) signaling pathway changed. We detected the RNA binding protein heterogeneous nuclear ribonucleoprotein L (HNRNPL) as a SPRY4-IT1 interacting protein through RNA pull-down assay and liquid chromatography-mass spectrometry, then verified through RNA immunoprecipitation. Downregulation of HNRNPL induced the change of proteins observed on SPRY4-IT1 downregulation revealing the SPRY4-IT1: HNRNPL complex in the TNF signaling pathway and EMT process in HCC. In general, our experimental data and analysis demonstrated the role of SPRY4-IT1 in promoting progress and metastasis of HCC by the TNF signaling pathway.
机译：我们先前的研究已经表明,长非编码RNA (IncRNA) SPRY4 intronic成绩单1 (SPRY4-IT1)是高度表达肝细胞癌(HCC)。仍不清楚SPRY4-IT1如何运作tumorgenesis肝癌。超表达在肝细胞癌组织和SPRY4-IT1细胞通过定量实时聚合酶连锁反应。upregulation有关联的肿瘤淋巴结转移阶段,凝血酶时间,碱性磷酸酶。可能参与细胞增殖,转移,epithelial-to-mesenchymal过渡(EMT)在肝细胞癌体外和过程vivo进行了探索的机制SPRY4-IT1肝癌。或过表达,蛋白质的水平肿瘤坏死因子(TNF)信号通路改变了。异构核L核糖核蛋白(HNRNPL)作为SPRY4-IT1相互作用的蛋白质通过RNA拉试验和液体相色谱-光谱法,然后验证通过RNA免疫沉淀反应。HNRNPL诱导的蛋白质的变化揭示了差别SPRY4-IT1对这些肿瘤坏死因子信号SPRY4-IT1: HNRNPL复杂通路在肝细胞癌和EMT过程。实验数据和分析证明了在促进进步和SPRY4-IT1的作用肝癌的转移肿瘤坏死因子信号通路。

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