Skip to main content
. 2019 Feb 20;16:105–117. doi: 10.1016/j.omtn.2019.02.008

Figure 5.

Figure 5

IGF-1R Knockdown-Triggered MDA5 and RIG-I Mediated Apoptosis through the Mitochondrial Pathway in Human Colonic Cancer Cells

(A) Annexin V-FITC-PI staining analysis showed increased apoptosis in HT-29 cells transfected with siIGF-1R and poly(I:C). Transfection of siMDA5 did not induce cell apoptosis. (B, a) HT-29 cell survival after treatment with poly(I:C), siIGF-1R, siMDA5, and IGF-1 for 48 h. Cell survival was strongly inhibited by the transfection of siIGF-1R and poly(I:C), but not siMDA5. IGF-1 significantly stimulated cell growth as compared to control cells. (B, b) HT-29 cell survival was dose-dependently inhibited with increasing concentrations of poly(I:C). Cells transfected with siIGF-1R (50 μM) achieved the same efficacy as poly(I:C). (C) JC-1 probe staining of HT-29 cells showed a loss of MMP in cancer cells with silenced IGF-1R, showing an increase of green fluorescence (second row), which was similar to the effect of poly(I:C) (third row). (D) Western blotting analysis showed increased Bim and cytochrome c in HT-29 cells with silenced IGF-1R (fourth lane). The efficacy of activated Bim and cytochrome c by silenced IGF-1R was higher than that by poly(I:C) (last lane). *p < 0.05, **p < 0.01, ***p < 0.001 versus NC cells.