MiR-144 Inhibits Proliferation and Induces Apoptosis and Autophagy in Lung Cancer Cells by Targeting TIGAR

被引:108
作者
Chen, Shanshan [1 ]
Li, Ping [1 ]
Li, Juan [1 ]
Wang, Yuanyuan [2 ]
Du, Yuwen [2 ]
Chen, Xiaonan [2 ]
Zang, Wenqiao [2 ]
Wang, Huaqi [1 ]
Chu, Heying [1 ]
Zhao, Guoqiang [2 ]
Zhang, Guojun [1 ]
机构
[1] Zhengzhou Univ, Affiliated Hosp 1, Dept Resp Med, Zhengzhou 450052, Peoples R China
[2] Zhengzhou Univ, Coll Basic Med Sci, Dept Microbiol & Immunol, Zhengzhou 450052, Peoples R China
关键词
Lung cancer cell; MiR-144; TIGAR; Proliferation; Apoptosis; EXPRESSION; MICRORNAS; CARCINOMA; INVASION; GLYCOLYSIS; REGULATOR;
D O I
10.1159/000369755
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
BACKGROUND: MiRNAs are noncoding RNAs of 20-24 nucleotides that function as post-transcriptional negative regulators of gene expression. MiRNA genes are usually transcribed by RNA polymerase II in the nucleus. Their initial products are pre-miRNAs which have cap sequences and polyA tails. The p53-induced glycolysis and apoptosis regulator (TIGAR) was discovered through microarray analysis of gene expression following activation of p53. However, little is known about the effect of miR-144 on cell proliferation and apoptosis and how it interacts with TIGAR. METHODS:We performed real-time PCR, western blotting, CCK8, colony formation, tumor growth, flow cytometry, Caspase3/7 activity, Hoechst 33342 staining, MDC staining of autophagic cells and luciferase reporter assays to detect the influence of miR-144 to lung cancer cells. RESULTS: miR-144 targeted TIGAR, inhibited proliferation, enhanced apoptosis, and increased autophagy in A549 and H460 cells. CONCLUSIONS: Our study improves our understanding of the mechanisms underlying lung cancer pathogenesis and may promote the development of novel targeted therapies. Copyright (C) 2015 S. Karger AG, Basel
引用
收藏
页码:997 / 1007
页数:11
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