KMT2D deficiency enhances the anti-cancer activity of L48H37 in pancreatic ductal adenocarcinoma

Figure 1 L48H37 inhibits proliferation and promotes apoptosis in pancreatic cancer cells. A-D: Percentage of viable SW1990, ASPC-1, PANC-1 and MIA PaCa₂ cells incubated with different concentrations of L48H37 (1.25, 2.5, 5, 10, 20 and 40 μmol/L) or DMSO (negative control) for 24, 48 and 72 h. The IC₅₀ values in the different cell lines are shown; E: Representative pictures of colonies from SW1990 and ASPC-1 cells treated with increasing concentrations of L48H37 for 24 h; F-G: SW1990 and Aspc-1 cells were treated with various concentrations of L48H37 for 24 h. Cell apoptosis was detected by flow cytometry. Histogram illustrating the rate of apoptosis cells. Data were expressed as mean ± SEM; F: ^bP < 0.01 vs L48H37 (0 μmol/L) group. ^dP < 0.01 vs L48H37 (10 μmol/L) group. ^fP < 0.01 vs L48H37 (15 μmol/L) group; G: ^bP < 0.01 vs L48H37 (0 μmol/L) group; ^dP < 0.01 vs L48H37 (5 μmol/L) group. ^fP < 0.01 vs L48H37 (10 μmol/L) group; H-I: Western blotting showing expression levels of Cleaved caspase3, Bcl-2 and Bax proteins in SW1990 and Aspc-1 cells following treatment with DMSO or L48H37 for 12 h. Grayscale values of Bcl-2 and Bax were measured relative to β-actin, and the ratio of Bcl-2/Bax expression was calculated. Data were expressed as mean ± SEM; H: ^bP < 0.01 vs L48H37 (0 μmol/L) group. ^dP < 0.01 vs L48H37 (10 μmol/L) group. ^fP < 0.01 vs L48H37 (15 μmol/L) group; I: ^bP < 0.01 vs L48H37 (0 μmol/L) group. ^dP < 0.01 vs L48H37 (5 μmol/L) group. ^fP < 0.01 vs L48H37 (10 μmol/L) group.