miR-448低表达通过调控ROCK2诱导肝癌细胞上皮-间质转化并促进其侵袭
Low Expression of miR-448 Induces EMT and Promotes Invasion by Regulating ROCK2 in Hepatocellular Carcinoma.
作者信息
Zhu Huaqiang, Zhou Xu, Ma Chaoqun, Chang Hong, Li Hongguang, Liu Fangfeng, Lu Jun
机构信息
Department of Hepatobiliary Surgery, Provincial Hospital Affiliated to Shandong University (East District), Jinan, China.
出版信息
Cell Physiol Biochem. 2015;36(2):487-98. doi: 10.1159/000430114. Epub 2015 May 11.
BACKGROUND/AIMS: miR-448 has been reported to exhibit abnormal expression in hepatocellular carcinoma (HCC), however, the essential role of miR-448 in HCC progression is still unclear.
METHODS
real-time PCR was used to detect the expression of miRNAs and candidate genes in HCC samples (n=117). miR-448 mimics and inhibitor were tansfected in human HCC cells. The transwell assay was used to examine the cell invasive ability. The regulation mechanism was confirmed by luciferase reporter assay. The markers of EMT were detected by using Western blot.
RESULTS
miR-448 was decreased in HCC samples and associated with HCC development. Inhibition of miR-448 significantly promoted cell invasion, while the effect of miR-448 up-regulation was reverse. miR-448 could regulate ROCK2 in hepatocellular carcinoma. Knockdown of ROCK2 expression partially reversed the effect of miR-448 inhibitor. Abnormal expression of miR-448 could regulate the markers of epithelial-mesenchymal transition (EMT).
CONCLUSIONS
miR-448 may contribute to the progression of HCC via regulating ROCK2 expression.
背景/目的：据报道，miR-448在肝细胞癌（HCC）中表达异常，然而，miR-448在HCC进展中的重要作用仍不清楚。
方法
采用实时定量PCR检测117例HCC样本中miRNA和候选基因的表达。将miR-448模拟物和抑制剂转染到人HCC细胞中。采用Transwell实验检测细胞侵袭能力。通过荧光素酶报告基因实验证实调控机制。采用蛋白质印迹法检测上皮-间质转化（EMT）标志物。
结果
HCC样本中miR-448表达降低，且与HCC发展相关。抑制miR-448可显著促进细胞侵袭，而miR-448上调的作用则相反。miR-448可在肝细胞癌中调控ROCK2。敲低ROCK2表达可部分逆转miR-448抑制剂的作用。miR-448的异常表达可调控上皮-间质转化（EMT）标志物。
结论
miR-448可能通过调控ROCK2表达促进HCC进展。
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