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. 2020 Nov 18;12(11):3413. doi: 10.3390/cancers12113413

Figure 6.

Figure 6

Role of mutant Kras in FL118-mediated apoptosis and inhibition of anti-apoptotic protein expression and cell viability. (A) Silencing of Kras G12C via Kras-specific shRNA in UMUC-3 cells increases cell resistance to FL118-induced apoptosis (less PARP cleavage). UMUC-3 cells were infected with Kras-specific lentiviral shRNA identified in our previous studies [21] or control shRNA followed by treatment with DMSO or FL118 (10 and 100 nM) for 24 h. At the end of treatment, Western blot analysis was performed to check PARP cleavage and the expression of anti-apoptotic proteins (XIAP, Mcl-1, survivin). GAPDH was used as an internal control. (B) 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was performed to determine cell viability with 10 nM and 100 nM FL118 treatment in UMUC-3 cells infected with control scramble shRNA and Kras-specific shRNA. Each bar in the histogram data is the mean ± SD from three independent assays. (C) Effect of forced expression of Kras G12V in HT1376 cells. HT1376 cells were transfected with Kras G12V or control vectors followed by treatment with DMSO or 100 nM FL118 for 48 h. At the end of treatment, Western blot analysis was performed to check the expression of apoptosis-related proteins. GAPDH was used as an internal control of total protein-loading. * p-value < 0.05.