Fig. 1: Activation of EMT and apoptosis in Camptothecin-mediated DNA damage response.
a HCT-116 and A549 cells were treated with 250 nM of CPT for 0, 12, 24, 36, and 48 h and checked for the expression of Vimentin, pser38Vimentin, Snail-1, ATM, β-catenin, and E-cadherin through western blot analysis. β-actin was used as loading control. b Immunocytochemistry was performed in HCT-116 cells treated with vehicle and CPT (250 nM) for 36 h for checking the expression of Vimentin, E-cadherin (green fluorescence). Nuclear staining was done with DAPI containing mounting media. Magnification of the images = ×63, c Analysis of the morphological features of HCT-116 cells through microscopic observation after exposure of cells to CPT for increasing time points (magnification = ×20). d Cells were treated with CPT (250 nM) for 24, 36, and 48 h along with vehicle and tested for their ability to degrade gelatin matrix and invadopodia formation through FITC-gelatin degradation assay. Blue stains indicate nuclear staining through DAPI mounting media. Images were taken at ×20 magnification. Bar graph showing the threshold area of degradation quantified through Image j analysis (n = 3, error bars ± s.d.). e, f Induced AhCre-ErT Apcfl/fl mice were treated with CPT (0.4, 0.8, and 12.2 mg/kg) for 24 and 48 h and the dissected intestinal tissues were sectioned and subjected to immunohistochemistry, to analyze the expression of Vimentin and pser38Vimentin. Images were taken at ×20 magnification
