406963

MIR187

miR-187-3p, a novel cancer-related microRNA, was previously reported to play promoting or suppressive roles in different malignancies. However, the expression level, biological function, and underlying mechanisms of miR-187-3p in hepatocellular carcinoma (HCC) remain unknown. This study demonstrated that miR-187-3p was significantly down-regulated in HCC tissues and cell lines, and was associated with advanced TNM stage and metastasis in HCC. Functional studies confirmed that miR-187-3p could inhibit the metastasis of HCC both in vitro and in vivo. Moreover, we proved that miR-187-3p could prevent the epithelial-mesenchymal transition (EMT) of HCC cells. Mechanically, S100A4 was a direct downstream target of miR-187-3p, and mediated the functional influence of miR-187-3p in HCC. Furthermore, miR-187-3p and S100A4 expression was evidently correlated with adverse clinical features and poor prognosis of HCC. Lastly, we showed that hypoxia was responsible for the significantly decreased level of miR-187-3p in HCC, and miR-187-3p was involved in the promoting effects of hypoxia on the metastasis and EMT of HCC cells. Taken together, miR-187-3p inhibits the metastasis and EMT in HCC by targeting S100A4. miR-187-3p can serve as a prognostic indicator and a promising therapeutic target for HCC patients.CI - Copyright (c) 2016 Elsevier Ireland Ltd. All rights reserved.

MicroRNAs (miRNAs) that negatively regulate gene expression play a key role in the development and progression of cancer. Aberrant expression of hsa-miR-187 (miR-187) has been reported in various malignancies. However, the function of miR-187 in tumor progression remains controversial and its role in non-small cell lung cancer (NSCLC) is poorly understood. In the present study, the role of miR-187 in the progression of NSCLC was investigated. Our results revealed that miR-187 was frequently upregulated in NSCLC tissues and cells. Furthermore, ectopic introduction of miR-187 promoted cell migration, whereas miR-187 inhibitor had the contrary effect in NSCLC cells. Of significance, miR-187 induced epithelial-mesenchymal transition (EMT), which plays a pivotal role in the initiation of metastasis and activated mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) pathways. Polymerase I and transcript release factor (PTRF) was identified as a direct target of miR-187 in the promotion of the migration of NSCLC cells. Restored expression of PTRF neutralized the promoting effect of miR-187 on cell migration and EMT of NSCLC cells. Collectively, our data highlight the pivotal role of miR-187 in the progression of NSCLC, indicating this factor as a potential candidate in molecular cancer therapy.