The fibroblast growth factor receptor (FGFR) is transmembrane tyrosine kinase receptor responsible for mediating cellular responses to FGFs signaling. They regulate a multitude of cellular processes, including cell growth, differentiation, migration and survival, and have been implicated in pathological processes including angiogenesis, wound healing and tumorigenesis. These receptors are widely expressed in many tissues and different cell types, and the temporal control of their expression is an important mechanism for regulating physiologically relevant signals. Here we have demonstrated that the gene expression of FGFR1 and FGFR3 in colorectal carcinoma cells is in reciprocal relationship. We have also showed that the disruption of FGFR1 expression by introducing of FGFR1 siRNA was effective in elevating FGFR3 expression and tumor suppressive activities. However, molecular details involved in such a switch are largely unknown. Nevertheless, to our knowledge, Therefore, FGFR1 may confer a selectable advantage on clones of cells in colorectal tumorigenesis, favoring proliferation, whereas FGFR3 may have the effect of an unfavorable negative regulation of progression of the carcinomas to malignancy, promoting differentiation.