Elevated CXCL1 increases hepatocellular carcinoma aggressiveness and is inhibited by miRNA-200a.
Elevated CXCL1 increases hepatocellular carcinoma aggressiveness and is inhibited by miRNA-200a.
复制标题
CXCL1 升高会增加肝细胞癌的侵袭性并被 miRNA-200a 抑制
DOI：
10.18632/oncotarget.11350
复制
发表时间：
2016-10-04
期刊：
影响因子：
--
通讯作者：
Zhu JY
中科院分区：
文献类型：
--
作者：
Cui X;Li Z;Gao J;Gao PJ;Ni YB;Zhu JY
在本研究中，我们探讨了趋化因子CXCL1在肝细胞癌（HCC）临床治疗中的价值及其在HCC分子发病机制中的可能作用。在体内和体外实验系统中，高表达的CXCL1预测HCC患者的复发并促进肿瘤进展。过表达CXCL1增加线粒体代谢，激活上皮-间质转化（EMT）。通过计算分析，我们确定了microRNA miR-200a是CXCL1的一个假定的转录后调节因子。我们通过northern blot和qRT-PCR发现HCC患者组织样本中miR-200a水平与CXCL1表达呈负相关。此外，CXCL1被鉴定为miR- 200a结合并抑制的直接靶点。这些发现为CXCL1在HCC中的作用及其转录后调控提供了新的见解，并表明它可能是预后不良的预后指标和潜在的治疗靶点。
In this study, we investigated the value of measurement of the chemokine CXCL1 in clinical management of hepatocellular carcinoma (HCC) and its possible role in the molecular pathogenesis of HCC. High CXCL1 expression predicted recurrence in HCC patients and promoted tumor progression in both in vivo and in vitro experimental systems. Overexpression of CXCL1 increased mitochondrial metabolism and activated the epithelial-to-mesenchymal transition (EMT). Using computational analysis we identified the microRNA miR-200a as a putative post-transcriptional regulator of CXCL1. We found that levels of miR-200a were inversely correlated with CXCL1 expression in HCC patient tissue samples by northern blot and qRT-PCR. Furthermore, CXCL1 was identified as a direct target which was bound and inhibited by miR- 200a. These findings provide new insights into the role of CXCL1 in HCC and its post-transcriptional regulation and suggest it may be a prognostic indicator for poor outcomes and a potential target for therapy.