Ma Teng, Zhao Ye, Wei Ke, Yao Guoliang, Pan Chunfeng, Liu Bin, Xia Yang, He Zhicheng, Qi Xiaotong, Li Zhi, Wang Jun, Shao Yongfeng
Cell Physiol Biochem. 2016;38(4):1563-74. doi: 10.1159/000443097. Epub 2016 Apr 14.
BACKGROUND/AIMS: Abnormal expression of microRNA-124 (miR-124) was found in non-small cell lung cancer (NSCLC). However, the association between miR-124 and CDH2 has not been reported yet. This study aims to reveal the inhibiting effects of miR-124 on the expression of CDH2 in NSCLC.
Quantitative real-time polymerase chain reaction was used to evaluate the expression of miR-124 and CDH2 in NSCLC tissues. Cell viability, apoptosis and invasion assays were carried out in NSCLC cell lines after transfection. The regulation mechanism was confirmed by luciferase report assay and western blot (WB).
Significantly decreased expression of miR-124 was found in NSCLC specimens and cell lines. Overexpression of miR-124 apparently suppressed the proliferation and invasion of NSCLC cell lines in vitro. Luciferase report assay and WB revealed that CDH2 was a target gene of miR-124. Furthermore, results of WB showed that epithelial-mesenchymal transition (EMT) could be inhibited by up-regulation of miR-124.
Taken together, our findings present the first evidence that miR-124 could suppress the expression of CDH2 and regulate EMT, which might lead to a potential therapeutic strategy focusing on miR-124 and CDH2 for human lung cancer.
背景/目的：在非小细胞肺癌（NSCLC）中发现了微小RNA-124（miR-124）的异常表达。然而，miR-124与CDH2之间的关联尚未见报道。本研究旨在揭示miR-124对NSCLC中CDH2表达的抑制作用。
采用定量实时聚合酶链反应评估NSCLC组织中miR-124和CDH2的表达。转染后在NSCLC细胞系中进行细胞活力、凋亡和侵袭实验。通过荧光素酶报告实验和蛋白质免疫印迹（WB）证实调控机制。
在NSCLC标本和细胞系中发现miR-124表达显著降低。miR-124的过表达明显抑制了NSCLC细胞系在体外的增殖和侵袭。荧光素酶报告实验和WB显示CDH2是miR-124的靶基因。此外，WB结果表明上调miR-124可抑制上皮-间质转化（EMT）。
综上所述，我们的研究结果首次证明miR-124可抑制CDH2的表达并调节EMT，这可能为人类肺癌提供一种针对miR-124和CDH2的潜在治疗策略。
