125I inhibited the NSCLC both in vivo and in vitro

Lung cancer is the main reason of cancer-linked death all over the world. Non-small cell lung cancer (NSCLC) patients always have an extremely poor prognosis. It is urgent to find novel treating methods. It was previously showed that 125 I brachytherapy had been applied to the lung cancer treatment. However, fundamental researches are limited. In the present study, we first explored the mechanism by which 125 I radiation induced arrest or apoptosis of the cell cycle and relevant protein expression. Furthermore, we explored its effect on the invasion. We found that 125 I significantly induced cell apoptosis through mitochondrial pathway, triggered S phase arrest via regulating cyclinA2, p21 and CDK6 expressions. Meanwhile, 125 I could inhibit invasion of NSCLC cells by altering the expression level of vimentin, N-cadherin and MMP-9. Furthermore, we confirmed the effects of 125 I on NSCLC cell growth in vivo. The results indicated that 125 I obviously inhibited the tumor growth. Thus, we determined that 125 I brachytherapy remarkably restrained NSCLC cellular growth and intrusion by inducing apoptosis, S phase arrest and corresponding protein expression.