| Literature DB >> 31938221 |
Weiliang Yan1, Xiaodong Huo2, Huixing Wang3, Bin Huo2, Yongtao Guo4, Hua Dong4, Guangjun Zheng1, Junjie Wang5, Shude Chai1, Haitao Wang2, Zuncheng Zhang4.
Abstract
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 125I 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 125I radiation induced arrest or apoptosis of the cell cycle and relevant protein expression. Furthermore, we explored its effect on the invasion. We found that 125I significantly induced cell apoptosis through mitochondrial pathway, triggered S phase arrest via regulating cyclinA2, p21 and CDK6 expressions. Meanwhile, 125I could inhibit invasion of NSCLC cells by altering the expression level of vimentin, N-cadherin and MMP-9. Furthermore, we confirmed the effects of 125I on NSCLC cell growth in vivo. The results indicated that 125I obviously inhibited the tumor growth. Thus, we determined that 125I brachytherapy remarkably restrained NSCLC cellular growth and intrusion by inducing apoptosis, S phase arrest and corresponding protein expression. IJCEPEntities:
Keywords: 125I; NSCLC; apoptosis; radioresistance
Year: 2018 PMID: 31938221 PMCID: PMC6958116
Source DB: PubMed Journal: Int J Clin Exp Pathol ISSN: 1936-2625