Co-introduction of an IGF1-R-expressing construct, or an activated form of Akt (myr-Akt), to HCT116 cells, partially blocked inhibition of cell viability by miR-497 mimics29 (Figures 4a and c), indicating that reduced cell viability in colon cancer cells when miR-497 is overexpressed is related to downregulation of IGF1-R and decreased activation of Akt signalling. This evidence concerns the gene IGF1R and colonic neoplasm.