Fig. 4: IGF-1R contributes to survival and recovery of 5-FU treated CRC cells.

a HCT116 cells were treated with 10 µM or 50 µM 5-FU for 24 h or 48 h or untreated (NT). Translation efficiency of actin, GAPGH and IGF-1R mRNAs. Each mRNA was quantified from cytoplasmic and polysomal fractions. Translation efficiency are shown as the ratio of polysomic mRNA over the cytoplasmic mRNA. Each dot represents an individual biological sample measured in duplicate and data are expressed as mean ± s.d of independent experiments (n = 3). b, c HCT116 cells were treated with 10 µM 5-FU for 24 h or 48 h or untreated (NT). b Cells were counted and an equivalent number of cells were loaded in each well. IGF-1R, Actin, GAPDH and H3 proteins were detected by western blot. c Level of IGF-1R, Actin, GAPDH and H3 proteins quantified from the western blot in b. Signals of each protein was normalized to the untreated (NT) value. Each dot represents an individual biological sample and data are expressed as mean ± s.d of independent experiments (n = 2). d, e HCT116 cells were treated with 10 µM 5-FU for 24 h or 48 h or NT, and not stimulated (No IGF-1) or stimulated with 5 or 10 ng/mL of IGF-1. Cell growth was monitored in real-time over 5 days. d Schematic representation of the experiment. e Growth rate measured over 72 h (day 6 to day 9). Each dot represents a technical replicate and data are expressed as mean ± s.d. f HCT116 cells were untreated (NT) or treated with 10 µM of 5-FU alone or with 5 µM of IGF-1R inhibitor NVP-AEW541 alone or with 10 µM of 5-FU for 48 h. Cell survival was assessed using MTS at 72 h post-treatment. Each dot represents a technical replicate and data are expressed as mean ± s.d. of independent experiments (n = 4). Results of unpaired two-tailed t test are indicated as nonsignificant (ns) p < 0.05 (*), p < 0.01 (**), p < 0.001 (***), and p < 0.0001 (****). Source data are provided as a Source Data file.