Abstract
Abstract Lung cancer is the leading cause of cancer related deaths worldwide. Delayed diagnosis and early metastasis are the major unsolved obstacles for most physicians in treating lung cancer patients. Thus, identifying novel metastatic genes and their action mechanisms involved in lung cancer progression and metastasis may provide new insights into the pathogenesis and management of lung cancer treatment. In a previous genome-wide gene expression profiling analysis using an invasion cancer cell lines model, we identified a panel of 589 genes whose expression was correlated with cell invasiveness. And Inhibitor of DNA binding 4 (Id4) was one of these candidates. In this study, we demonstrate that the expression of Id4 was inversely associated with cell invasiveness in different lung cancer cell lines. Through manipulating the expression of Id4, we found that the expression of Id4 not only attenuate cell migration and invasion in vitro, but also affect the regulation of Epithelial-mesenchymal transition (EMT), a critical step for cancer metastasis. Additionally, we demonstrated that the expression Id4 was inversely correlated with lung cancer metastasis in vitro and in vivo and the reason Id4 affects metastasis probably is the regulation of EMT procession. Our data showed that Id4 could regulate EMT pathway by controlling the expression of Slug, a well-known EMT regulator, and recovering promoter activity of E-cadherin. Collectively, Id4 is a tumor suppressor in lung cancer, it can down-regulate EMT by reversing E-cadherin expression that represses by Slug. How to translate this research result for clinical application and develop potential therapeutic strategy for lung cancer treatment is our work in the future. Citation Format: Szu-Hua Pan, Yuan Ling Hsu, Pei-Fang Hung, Chia-Jen Wang, Chi-Chung Wang. Id4 inhibits cancer metastasis through EMT regulation in lung cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1431. doi:10.1158/1538-7445.AM2015-1431
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