Supplementary Figure Legends s12

Supplementary Figure legends:

Fig. 1a Histograms showing the relative values of DCF fluorescence on FL1-H scale (x-axis) with cell count (y-axis). Markers were set according to the control population with blank correction.

Fig. 1b Graph represents the mean fluorescent intensity (MFI) of DCF (all 104 events) in different groups. NSAIDs co-administered groups are having higher MFI as compared to

DMH supporting that in-total lower ROS is essential for tumorigenesis. The values are Mean

± S.D. of 3 independent experiments with 4 different animals from each group. bp≤0.01 and cp≤0.001 in comparison to control, zp≤0.001 in comparison to DMH by one way ANOVA.

Fig. 2a Histograms showing the relative values of R123 fluorescence on FL2-H scale (x-axis) with cell count (y-axis). Markers were set according to control population with blank correction.

Fig. 2b Graph representing the overall MFI of R123 fluorescence with a significant reduction of MMP in DMH + Sulindac and DMH + Celecoxib groups as compared to DMH group.

Sulindac treatment is showing significant reduction of MMP as compared to Celecoxib. The values are Mean ± S.D. of 3 independent experiments with 4 different animals from each group. ap≤0.05, bp≤0.01 and cp≤0.001 in comparison to control, zp≤0.001 in comparison to

DMH, ep≤0.05 in comparison to DMH + Sulindac by one way ANOVA.

Fig. 3 Contour plots showing the distribution of colonocytes according to the J-aggregates

(high MMP with red fluorescence on FL2-H), monomers (low MMP with green fluorescence on FL1-H) and heterogenic population (orange). Markers were set according to the control with blank correction.

Fig. 4 Molecular docking analysis of Bcl-xL (PDB ID: 3QKD; represented with space filling

CPK model) with Sulindac and Celecoxib (both represented with wire model, respectively) showing the docked complexes at the inhibitor binding site of Bcl-xL molecule. These structures also show the putative amino acid residues of the binding site which could interact with the drug molecules via H-bonds.