Suppression of nucleosome-binding protein 1 by miR-326 impedes cell proliferation and invasion in non-small cell lung cancer cells

被引:28
|
作者
Li, Dongfan [1 ]
Dui, Xusheng [1 ]
Liu, An [1 ]
Li, Peng [2 ]
机构
[1] Xi An Jiao Tong Univ, Xian Cent Hosp, Dept Respirat Med, Xian 710004, Shaanxi, Peoples R China
[2] Xi An Jiao Tong Univ, Affiliated Hosp 2, Dept Pediat Surg, Xian 710004, Shaanxi, Peoples R China
关键词
NSBP1; miR-326; non-small cell lung cancer; cell proliferation; cell invasion; DOMAIN; 5; CLINICAL-SIGNIFICANCE; MICRORNA SIGNATURES; IN-VITRO; EXPRESSION; KNOCKDOWN; BIOGENESIS; PROMOTES; SURVIVAL; TARGET;
D O I
10.3892/or.2015.4403
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Emerging studies have proposed microRNAs (miRNAs) as novel therapeutic tools for cancer therapy. Nucleosome-binding protein 1 (NSBP1) has been suggested as an oncogene in various types of human cancers. The present study aimed to identify a novel miRNA that could directly target and negatively modulate NSBP1 expression. We found that NSBP1 was highly expressed in non-small cell lung cancer (NSCLC) cells, and knockdown of NSBP1 by NSBP1 small interfering RNA (siRNA) significantly suppressed NSCLC cell proliferation and invasion. Bioinformatics analysis revealed that miR-326 had a putative binding site within the 3'-untranslated region of NSBP1. Their substantial relationship was further verified by dual-luciferase reporter assay, real-time quantitative polymerase chain reaction and western blot analysis. Overexpression of miR-326 significantly inhibited NSCLC cell proliferation and invasion, which mimicked the effect of NSBP1 siRNA. Furthermore, suppression of NSBP1 by NSBP1 siRNA or miR-326 overexpression remarkably repressed the expression of cyclin B1 and matrix metalloproteinase 9 (MMP9), which are associated with cancer cell proliferation and invasion. Moreover, overexpression of NSBP1 obviously abolished the inhibitory effect of miR-326 on cyclin B1 and MMP9 expression. In addition, an inverse correlation between miR-326 and NSBP1 expression levels was found in NSCLC clinical specimens. Our study demonstrated a direct target relationship between NSBP1 and miR-326 through which miR-326 inhibited cell proliferation and invasion of NSCLC cells. Thus, miR-326-NSBP1 is a promising candidate target for developing novel anticancer therapeutics for NSCLC.
引用
收藏
页码:1117 / 1124
页数:8
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