Figure 2

R2 is a lead compound targeting FAK-p53 interaction. A. The viability MTT assay with HCTp53⁺/⁺ and HCTp53^-/^- cells identified small molecules, called R compounds that significantly decreased the viability of HCT116 p53⁺/⁺ cells compared with HCT116p53^-/^- cells. * P<0.05 viability less in HCT116p53⁺/⁺ cells versus HCT116 p53^-/^- cells. B. R2 significantly decreased cancer cell clonogenicity in a p53-dependent manner. The compound R2 decreased clonogenicity in HCT116p53⁺/⁺ cells more significantly than in HCT116p53^-/^- cells. C. The structure of R2 compound. D. The R2 compound decreased cancer cell viability in a p53-and dose-dependent manner. MTT assay with different doses of R2 compound was performed in HCT116p53⁺/⁺ and HCT116p53^-/^- cells. *p<0.05, R2-treated HCT116p53⁺/⁺ versus HCT116 p53^-/^- cells. E, F. R2 compound decreased the viability of cancer cell lines with wild type p53 more efficiently than with mutant p53. MTT assay was performed with different doses of R2 in MCF-7 (wild type p53) (E) and MDA231 (mutant p53) (F) breast cancer cells. * p<0.05 treated with R2 versus untreated cells. G. MTT assay with R2 in pancreatic cancer cell line, Miapaca-2 cells (mutant p53). H. MTT assay with R2 in normal human WI 38-hTERT fibroblasts. The MTT assay was performed as in Figure 2 E, F.