Abstract 5295: S100A4 regulates tumor growth, motility, and invasion in pancreatic cancer

Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC S100A4 protein belongs to the S100 subfamily, which has grown to be one of the large subfamilies of the EF-hand Ca2+-binding proteins, and overexpression of S100A4 is suggested to associate with cell proliferation, invasion, and metastasis. We observed frequent overexpression of S100A4 in pancreatic cancer cell lines by quantitative real-time RT-PCR and Western blotting. Tissue microarray analysis validated S100A4 overexpression in primary pancreatic cancer tissues, and overexpression of S100A4 associated with perineural invasion. We further analyzed RNAi-mediated knockdown to address the possibility of its use as a therapeutic target for pancreatic cancer. The specific knockdown of S100A4 strongly suppressed cell growth, induced G2 arrest and eventual apoptosis, and decreased cell migration. Furthermore, microarray analyses revealed that knockdown of S100A4 induced expression of the tumor suppressor genes PRDM2 and VASH1. We further established stably S100A4-expressing cell lines using two pancreatic cancer cell lines with low level of S100A4 expression; remarkable accelerated cell growth and motility was observed after induction of S100A4, whereas no change was observed in the control cells. Comparison of the expressional profiles after siRNA-mediated knockdown and expression vector-mediated induction is underway, and the results will also be demonstrated and discussed. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5295.