p100 functions as a metastasis activator and is targeted by tumor suppressing microRNA‐320a in lung cancer

BACKGROUND Lung cancer is among the most frequently diagnosed types of cancer worldwide, with high morbidity and mortality. Metastasis accounts for the deadliest and most poorly understood feature of lung cancer. Herein, we demonstrate that SND1 (also known as p100) acts as a candidate metastasis activator and is targeted by microRNA-320a (miR-320a) in lung cancer cells. METHODS p100 expression in lung cancer cell lines and tissues was determined by quantitative real time-PCR and Western blot. RNA interference was applied to investigate the functions of p100 in lung cancer cell migration, reflected by wound healing and transwell assays. Luciferase reporter assay, quantitative real time-PCR, and Western blot were finally used to examine miR-320a targeting of p100 in lung cancer cells. RESULTS p100 expression was significantly higher in lung cancer cell lines and tissues compared to normal human bronchial epithelial cells and matched normal lung tissues. Downregulation of p100 by RNA interference obviously inhibited lung cancer cell migration in vitro. Moreover, we validated p100 as a direct target of miR-320a, a tumor suppressing microRNA repressing lung cancer cell migration. Finally, we showed an inversely expressed correlation between p100 and miR-320a in tested lung cancer tissues and cell lines, both of which acted as important prognostic factors in lung cancer. CONCLUSION Our findings identify that p100, targeted by tumor suppressing miR-320a, is a key metastasis activator in lung cancer, and both p100 and miR-320a could be considered as biomarkers for prognosis of lung cancer patients.