微小RNA-599通过SATB2促进非小细胞肺癌细胞侵袭。
The miR-599 promotes non-small cell lung cancer cell invasion via SATB2.
作者信息
Tian Wenjun, Wang Guanghai, Liu Yiqing, Huang Zhenglan, Zhang Caiqing, Ning Kang, Yu Cuixiang, Shen Yajuan, Wang Minghui, Li Yuantang, Wang Yong, Zhang Bingchang, Zhao Yaoran
机构信息
Department of Clinical Laboratory, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China.
Department of Respiratory Medicine, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, China.
出版信息
Biochem Biophys Res Commun. 2017 Mar 25;485(1):35-40. doi: 10.1016/j.bbrc.2017.02.005. Epub 2017 Feb 4.
MicroRNAs (miRNAs) play important roles in the pathogenesis of many types of cancers by negatively regulating gene expression at posttranscriptional level. Here, we identified that miR-599 is up-regulated in non-small cell lung cancer (NSCLC) patients. It promoted NSCLC cell proliferation by negatively regulating SATB2. In NSCLC cell lines, CCK-8 proliferation assay indicated that the cell proliferation is promoted by miR-599 mimics. Transwell assay showed that miR-599 mimics promoted the invasion and migration of NSCLC cells. Luciferase assays confirmed that miR-599 directly binds to the 3'untranslated region of SATB2, and western blotting showed that miR-599 suppresses the expression of SATB2 at the protein level. This study indicates that miR-599 promotes proliferation and invasion of NSCLC cell lines via SATB2. The miR-599 may represent a potential therapeutic target for NSCLC treatment.
微小RNA（miRNA）通过在转录后水平负向调节基因表达，在多种癌症的发病机制中发挥重要作用。在此，我们发现miR-599在非小细胞肺癌（NSCLC）患者中上调。它通过负向调节SATB2促进NSCLC细胞增殖。在NSCLC细胞系中，CCK-8增殖试验表明miR-599模拟物促进细胞增殖。Transwell试验显示miR-599模拟物促进NSCLC细胞的侵袭和迁移。荧光素酶试验证实miR-599直接与SATB2的3'非翻译区结合，蛋白质印迹显示miR-599在蛋白质水平抑制SATB2的表达。本研究表明，miR-599通过SATB2促进NSCLC细胞系的增殖和侵袭。miR-599可能是NSCLC治疗的潜在治疗靶点。
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