Extended Data Fig. 6: Additional characterization of the role of ACSS2 in tumor cell survival under normal pH.
a, Relative survival of S2-013, HPAF-II, CFPAC-1, and T3M4 cells upon treatment with 20 µM ACSS2 inhibitor, without and with acetate, for 72 hrs under normal pH conditions. The cell survival is normalized to the respective untreated controls. (n = 3 for S2-013, n = 6 for HPAF-II, n = 8 for CFPAC-1, n = 3 for T3M4 in each group from independent biological replicates). b, The relative survival of scrambled control (siScr) and ACSS2 knockdown (siACSS2) S2-013, HPAF-II, CFPAC-1, and T3M4 cells cultured in the presence and absence of acetate for 72 hrs under normal pH conditions. The cell survival is normalized to the respective untreated controls. (n = 3 for S2-013, n = 6 for HPAF-II, n = 3 for CFPAC-1, n = 3 for T3M4 in each group from independent biological replicates). c, The relative survival of scrambled control (shScr) and ACSS2 knockdowns (shACSS2-a and shACSS2-b) S2-013, HPAF-II, and CFPAC-1 cells cultured in the presence and absence of acetate for 72 hrs under normal pH conditions. The cell survival is normalized to the respective untreated controls. (n = 3 for S2-013, n = 3 for HPAF-II, n = 8 for CFPAC-1 in each group from independent biological replicates). Two-way ANOVA with Tukey’s post-hoc test; mean ± s.e.m. (a,b,c).
