MICRORNA-23B INHIBITS NON-SMALL CELL LUNG CANCER PROLIFERATION, INVASION AND MIGRATION VIA DOWNREGULATION OF RUNX2 AND INHIBITION OF WNT/B-CATENIN SIGNALING PATHWAY

被引:0
|
作者
Wang, H-X [1 ]
Wang, X-Y [2 ]
Fei, J-W [1 ]
Li, F-H [1 ]
Han, J. [1 ]
Qin, X. [1 ]
机构
[1] Yantaishan Hosp, Dept Resp Med, 91 Jiefang Rd, Yantai 264000, Peoples R China
[2] Jinan Zhangqiu Dist Hosp TCM, Dept Clin Lab, Jinan, Peoples R China
关键词
NSCLC; miR-23b; RUNX2; Wnt/beta-catenin; METASTASIS; BIOLOGY;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Non-small cell lung cancer (NSCLC) accounts for about 85% of all lung cancer cases. MicroRNAs (miRNAs/miRs) have been reported to play significant roles in the progression of human tumors, however, the expression and biological role of miR-23b in NSCLC remains elusive. Underexpression of miR-23b was detected in NSCLC tissues in comparison with the matched para-carcinoma tissues. The clinical value of miR-23b was analyzed, and the findings showed that miR-23b expression was negatively correlated with poor overall survival and malignant clinicopathologic characteristics of NSCLC patients. Furthermore, functional assays demonstrated that overexpression of miR-23b inhibited NSCLC cell viability, invasion and migration. Luciferase reporter assay and qRT-PCR revealed that RUNX2 was a functional target of miR-23b. The elevated expression of RUNX2 was positively correlated with overall survival of NSCLC patients. Additionally, Western blot analysis indicated that EMT and Wnt/beta-catenin pathways were blocked by the upregulation of miR-23b. Taken together, these data demonstrated that dysregulation of miR-23b/RUNX2 signal may be a novel therapeutic target for the treatment of NSCLC.
引用
收藏
页码:825 / 835
页数:11
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