Vimentin activation in early apoptotic cancer cells errands survival pathways during DNA damage inducer CPT treatment in colon carcinoma model

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 magnificatio