Zhang Xiao-Wen, Liu Ning, Chen Sheng, Wang Y E, Sun Kai-Lai, Xu Zhen-Ming, Fu Wei-Neng
Department of Medical Genetics, China Medical University, Shenyang, Liaoning 110001, P.R. China.
Department of Otolaryngology, No. 463 Hospital of PLA, Shenyang, Liaoning 110007, P.R. China.
Oncol Lett. 2015 Jul;10(1):410-416. doi: 10.3892/ol.2015.3238. Epub 2015 May 20.
MicroRNA-23a (miR-23a) is a potential biomarker for laryngeal cancer. Apoptotic protease activating factor 1 ( was recently demonstrated to be a target of miR-23a. However, whether miR-23a exerts its effects via in laryngeal cancer, remains unknown. In the present study, miR-23a expression was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). mRNA and protein expression levels were assayed by RT-qPCR and western blotting, respectively. Binding of miR-23a to was monitored by a luciferase reporter assay. Gain-of-function and loss-of-function studies were performed in order to investigate the roles of miR-23a and in Hep2 cell proliferation and apoptosis. miR-23a and were found to be significantly upregulated and downregulated, respectively, in laryngeal cancer tissues, and there was a significant negative correlation between and miR-23a expression. The results of the luciferase reporter assay demonstrated that miR-23a bound directly to the mRNA 3'-untranslated region. Ectopic expression of miR-23a and knockdown of significantly promoted cell proliferation and colony formation, and inhibited early apoptosis in Hep2 cells. In conclusion, miR-23a acts as an oncogenic regulator in laryngeal carcinoma by directly targeting , and may be a useful biomarker in the diagnosis and treatment of laryngeal carcinoma.
微小RNA-23a(miR-23a)是喉癌的一种潜在生物标志物。凋亡蛋白酶激活因子1(最近被证明是miR-23a的一个靶标。然而,miR-23a在喉癌中是否通过 发挥其作用仍不清楚。在本研究中,通过逆转录-定量聚合酶链反应(RT-qPCR)检测miR-23a的表达。分别通过RT-qPCR和蛋白质印迹法检测 mRNA和蛋白质表达水平。通过荧光素酶报告基因检测监测miR-23a与 的结合。进行功能获得和功能丧失研究以探讨miR-23a和 在Hep2细胞增殖和凋亡中的作用。发现miR-23a和 在喉癌组织中分别显著上调和下调,并且 与miR-23a表达之间存在显著负相关。荧光素酶报告基因检测结果表明,miR-23a直接与 mRNA的3'非翻译区结合。miR-23a的异位表达和 的敲低显著促进了Hep2细胞的增殖和集落形成,并抑制了早期凋亡。总之,miR-23a通过直接靶向 在喉癌中作为一种致癌调节因子,并且可能是喉癌诊断和治疗中的一种有用生物标志物。