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

Abstract

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 miR326 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 miR326 significantly inhibited NSCLC cell proliferation and invasion, which mimicked the effect of NSBP1 siRNA. Furthermore, suppression of NSBP1 by NSBP1 siRNA or miR326 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 miR326 on cyclin B1 and MMP9 expression. In addition, an inverse correlation between miR326 and NSBP1 expression levels was found in NSCLC clinical specimens. Our study demonstrated a direct target relationship between NSBP1 and miR326 through which miR326 inhibited cell proliferation and invasion of NSCLC cells. Thus, miR326NSBP1 is a promising candidate target for developing novel anticancer therapeutics for NSCLC.