Skip to main content
. 2016 Mar 2;7(12):14841–14856. doi: 10.18632/oncotarget.7854

Figure 3. Measurements of CIN induced through treatment by anticancer agents or gene knockouts.

Figure 3

A., B. Effect of anticancer drugs on CIN was measured by “gain of signal” and “loss of signal” HAC-based assays. HT1080 cells containing either the mCherry-shRNA-HAC or EGFP-HAC were treated by ten different compounds as described in MATERIALS AND METHODS. The rate of HAC loss per cell division was calculated based on the ratio of HAC-positive, HAC-negative cells and the average time per cell division. The drug concentrations used were at IC50 for HT1080 cells. The strongest CIN inducers identified were gemcitabine, taxol, PF-2771 and GSK923295. The control corresponds to the frequency of spontaneous HAC loss in HT1080 cells. C., D. Effect of gene knockouts on the rate of HAC loss. HT1080 cells carrying either the mCherry-shRNA-HAC or EGFP-HAC were treated by different siRNAs and the rate of HAC loss per generation was calculated as described in MATERIALS AND METHODS. In both systems, the strongest CIN effect was observed after cells treatment with MIS18β siRNA. The control corresponds to a frequency of HAC loss after treatment by a negative control siRNA.