Activated STAT3 may participate in tumor progression through increasing CD133/survivin expression in early stage of colon cancer. 
The activation of signal transducer and activator of transcription 3 (STAT3) by elevated interleukin (IL) levels has been reported to regulate tumorigenesis both in vitro and in vivo.  However, the clinical implication of p-STAT3 expression in colon cancer is still controversial.  In this study, we evaluated the effect of STAT3 inactivation on biologic behavior of primary (Caco-2) and metastatic colon cancer cells (LoVo and SNU407) and the relation of p-STAT3 expression with the invasion of colon tumor.  In vitro study, the STAT3 inhibition by siRNA and stattic treatment significantly reduced colony formation and cell migration and decreased CD133 and survivin the expression compared with a control in all three cell lines.  Furthermore, primary cancer cells exhibited a marked decrease in CD133 expression and increased apoptosis compared to metastatic cells after stattic treatment.  The immunohistochemical assay using clinical samples of colonic tumors with various invasion depth showed that p-STAT3 expression was inversely associated with tumor invasion (p = 0.001, hazard ratio (HR) = 0.328, 95% confidence interval (95%CI): 0.170-0.632).  In conclusion, p-STAT3 may participate in the progression of the early stage of colon cancer through the up-regulation of CD133, which in turn induces survivin expression.  However, the regulatory mechanism of these molecules in tumor progression in vivo is need to be more verified.