Abstract
A cell surface antigen CD133 is widely regarded as a stem cell marker and tumor initiating cells. However, the expression mechanism, biological functions and roles in cancer cells of CD133 largely remain unclear. The aim of this study is to investigate the regulation of expression of CD133 in cancer cells. We examined the expression of CD133 in cancer cell line and detected the moderate expressions by real time RT-PCR and Western blot on several gastrointestinal cancer cell lines. We hypothesized that the expression of CD133 in cancer cells was affected by uncontrolled signaling transduction, in particular tyrosine kinases. We examined the expression status of CD133 using real time PCR or western blot under the several cytotoxic and molecular target agents. The mTOR inhibitor, rapamycin dose-dependently increased the expression of CD133. EGFR-tyrosine kinase inhibitor, PI3K inhibitor, LY294002 and wortmannin also increased the expression of CD133. In consequence, we focused on mTOR signaling and the expression. Luciferase reporter assay of CD133 demonstrated that rapamycin increased the level of luciferase activity. These results suggest that mTOR signaling plays an important role of CD133 expression in cancer cell line.
Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 1079.
100th AACR Annual Meeting-- Apr 18-22, 2009; Denver, CO