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Accumulating evidence indicates that Voltage Dependent Anion Channel 1 (VDAC1) correlates with the initiation and progression of non-small cell lung cancer (NSCLC). However, the regulatory mechanism of VDAC1 in NSCLC remains unclear. Previous studies have reported that expression of miR-320a was decreased in human primary squamous cell lung carcinoma, which prompted us to investigate whether there is a functional link between decreased miR-320a and a high expression of VDAC1. In the present report, using computational analysis, we first show that miR-320a has a potential binding site on VDAC1 mRNA, and expression of miR-320a was decreased in NSCLC cell lines. Using gain-of-function and rescue experiments, we demonstrate that VDAC1 is a direct target of miR-320a in NSCLC cells, and miR-320a inhibits VDAC1 expression in NSCLC cells. Further we show that MiR-320a was significantly decreased in NSCLC tissues compared with adjacent non-tumor tissues, and MiR-320a level is negatively correlated with VDAC1 in NSCLC tissues by Pearson's correlation coefficient analysis. Moreover, using cellular ATP assay, we found that suppression of VDAC1 expression may inhibit cell proliferation and invasion of NSCLC by decreasing cell energy and metabolism. Importantly, we showed that ectopic overexpression of miR-320a blocked tumor cell proliferation and invasion, both in vitro and in vivo, through inhibiting VDAC1. Our results suggest that reduced expression of miR-320a facilitates the development of NSCLCs by increasing VDAC1 expression. We identified a novel regulatory mechanism between miR-320a and VDAC1, and miR-320a may serve as a tumor suppressor gene and a promising therapeutic target of NSCLCs.

Decreased expression of microRNA-320a promotes proliferation and invasion of non-small cell lung cancer cells by increasing VDAC1 expression