Abstract The glycoprotein carcinoembryonic-antigen-related cell adhesion molecule 1 (CEACAM1) is a membrane-bound protein found in microvilli of the apical colon cell surface. Recently, It was reported that signal transduction through the cytoplasmic domains appears to be important for the tumor suppressor function of CEACAM1 and also apoptosis induction in early tumor development. However, the mechanisms that control CEACAM1 expression are not clear. In this study, we show that CEACAM1 expression is induced in a p53-dependent manner. More importantly, alternative splicing of CEACAM1 to the long form (CEACAM1-4L) and the short form (CEACAM1-4S) is regulated by p53 in human colon carcinoma cells, Hct116. Treatment with etoposide induced CEACAM1 expression in cells that have p53 function, but not in cells lacking p53 function. In addition, knockdown of endogenous wild-type p53 using RNA interference and p53 overexpression by adenoviral vector were paralleled with CEACAM1 expression in Hct116 cells. These results suggest that induction of CEACAM1 in the context of tumor suppression is regulated in a p53-dependent manner and implicate CEACAM1 as a key determinant of cell fate. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. 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 1106.