High expression of RBM8A predicts poor patient prognosis and promotes tumor progression in hepatocellular carcinoma
High expression of RBM8A predicts poor patient prognosis and promotes tumor progression in hepatocellular carcinoma
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RBM8A的高表达预示患者预后不良并促进肝细胞癌的肿瘤进展
DOI：
10.3892/or.2017.5457
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发表时间：
2017-04-01
期刊：
影响因子：
4.2
通讯作者：
Ye, Hai-Hong
中科院分区：
文献类型：
--
作者：
Liang, Rong;Lin, Yan;Ye, Hai-Hong
肝细胞癌（HCC）是全球范围内对人类健康的巨大威胁。肝癌是一种复杂的肿瘤，其发生发展尤其是转移的分子基础有待进一步研究。尽管RNA结合基序（RBM）蛋白与多种癌症密切相关，但RBM 8A在HCC中的临床重要性和潜在机制仍不清楚。在这项研究中，我们发现RBM 8A在HCC肿瘤组织中的表达高于正常肝组织。RBM 8A过表达与HBsAg和Edmondson病理分级相关。Kaplan-Meier生存分析显示RBM 8A高表达与HCC患者的总生存期和无进展生存期相关。功能获得和丧失实验进一步证明RBM 8A通过激活上皮-间质转化信号通路促进HCC中肿瘤细胞的迁移和侵袭。还值得注意的是，RBM 8A是HCC中肿瘤细胞增殖和抗凋亡所需的。总之，我们的研究结果揭示了RBM 8A与HCC预后的密切关系，以及RBM 8A在HCC进展中的关键促肿瘤作用，表明RBM 8A可能是HCC治疗的潜在生物标志物和药物靶点。
Hepatocellular carcinoma (HCC) is a huge threat for human health worldwide. As a complicated tumor, the molecular basis for HCC development especially metastasis requires exploration. Although RNA binding motif (RBM) proteins are closely related to various cancers, the clinical importance and underlying mechanisms of RBM8A in HCC remain elusive. In this study, we found that RBM8A was highly expressed in HCC tumor tissues compared to normal liver tissues. Overexpression of RBM8A was associated with HbsAg and Edmondson pathological grading. Moreover, Kaplan-Meier survival analysis showed that high expression of RBM8A was related to the poor overall survival and progression-free survival of patients with HCC. Gain- and loss-of-function experiments further demonstrated that RBM8A promoted tumor cell migration and invasion in HCC via activation of epithelial-mesenchymal transition signaling pathway. It is also noteworthy that RBM8A is required for tumor cell proliferation and anti-apoptosis in HCC. Altogether, our results revealed a close relationship between RBM8A and HCC prognosis as well as a critical tumor-promoting function of RBM8A in HCC progression, suggesting that RBM8A might be a potential bio-marker and drug target in HCC therapy.