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. Author manuscript; available in PMC: 2017 Jul 1.

Published in final edited form as: J Surg Res. 2016 Apr 22;204(1):47–54. doi: 10.1016/j.jss.2016.04.021

A) I3C treatment of DLD1, HCT116, HT-29, LS513, and RKO cells lead to a dose-dependent decrease in cell viability. Cells were treated with I3C (100 μM, 500 μM, 1 mM) for 24 hours and cell viability was measured using a metabolically activated fluorogenic substrate. Data are depicted as mean viability percentage ± standard error, as normalized by DMSO treated control groups (representing at least three discrete experiments). “*” indicates statistical significance between I3C treated cell viability levels and vehicle (DMSO) controls in all cell types (p<0.05). B) Light microscope representation of 24 hour I3C treatment in all colorectal cancer cancer cell types. Images of monolayer cells are depicted with both vehicle (DMSO) and 1 mM I3C treatment at 24 hours. I3C treatment induced widespread pyknosis and fragmentation as compared to controls. C) I3C treatment stimulated apoptotic activity in all tested cell lines. Cells were treated with 1 mM I3C and luminescent caspase-3/7 activity was measured at 24 hours. Data are depicted as mean percentage of caspase-3/7 activity over DMSO treated controls ± standard error (representing at least three discrete experiments). “*” indicates statistical significance between I3C treated apoptotic activity levels and vehicle (DMSO) controls in all cell types (p<0.05).

A) I3C treatment of DLD1, HCT116, HT-29, LS513, and RKO cells lead to a dose-dependent decrease in cell viability. Cells were treated with I3C (100 μM, 500 μM, 1 mM) for 24 hours and cell viability was measured using a metabolically activated fluorogenic substrate. Data are depicted as mean viability percentage ± standard error, as normalized by DMSO treated control groups (representing at least three discrete experiments). “*” indicates statistical significance between I3C treated cell viability levels and vehicle (DMSO) controls in all cell types (p<0.05). B) Light microscope representation of 24 hour I3C treatment in all colorectal cancer cancer cell types. Images of monolayer cells are depicted with both vehicle (DMSO) and 1 mM I3C treatment at 24 hours. I3C treatment induced widespread pyknosis and fragmentation as compared to controls. C) I3C treatment stimulated apoptotic activity in all tested cell lines. Cells were treated with 1 mM I3C and luminescent caspase-3/7 activity was measured at 24 hours. Data are depicted as mean percentage of caspase-3/7 activity over DMSO treated controls ± standard error (representing at least three discrete experiments). “*” indicates statistical significance between I3C treated apoptotic activity levels and vehicle (DMSO) controls in all cell types (p<0.05).