Abstract 5265: S100P increases Twist expression and triggers FAK/AKT signaling in lung cancer

Abstract

Abstract Lung cancer accounts for 12% of all new cases of cancers worldwide and is the leading cause of cancer-related death. S100P, a calcium binding protein, has been reported to involve in cancer metastasis. However, the role of S100P is poorly known in lung cancer. This study first reports that S100P enhances the migration and invasion ability of lung cancer cells through the Twist1 upregulation and FAK (focal adhesion kinase)/Src/AKT signaling pathway. Compared to low invasive CL1-0, the expression of S100P is greater in that of high invasive CL1-5 cells. Overexpression of S100P increases the migration and invasion in CL1-0 cells, whereas knockdown of S100P expression decreases the migration and invasion of CL1-5 cells. Enhancement of S100P expression triggers FAK activation, which in turn increases the activation of Src and AKT signaling. Blockade of FAK by specific inhibitor prevents S100P-mediated cell migration and invasion. In the other hand, S100P also increases Twist1, which is responsible for epithelial-mesenchymal transition in lung cancer. More important, elevated expression of S100P protein was also found in human lung cancer specimen. This study demonstrates that S100P may be a novel anticancer target gene for the prevention of non-small cell lung cancer metastasis. In other way, it also can be a biomarker for prognosis of lung cancer metastasis. Citation Format: Yung-Yu Liang, Po-Lin Kuo, Ya-Ling Hsu. S100P increases Twist expression and triggers FAK/AKT signaling in lung cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 5265. doi:10.1158/1538-7445.AM2014-5265