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. 2024 Nov 1;10(44):eado6765. doi: 10.1126/sciadv.ado6765

Fig. 6. COX20 is a dependency factor in T-ALL.

Fig. 6.

(A) Western blot analysis (top) and quantification (bottom) of COX20 and Actin (loading control) levels upon knockdown of COX20 in Jurkat at 72 hours. (B and C) In vitro proliferation assays, in Karpas-45 (B) and Jurkat (C), demonstrate that loss of COX20 expression has a negative effect on cell proliferation rate (n = 3, two-way ANOVA). (D) Similar to the knockdown of PSIP1, annexin-7AAD stainings demonstrate that loss of COX20 expression in a cell line with a KMT2Ar (Karpas-45) induces apoptosis, while this is not the case for a non-KMT2Ar cell line (Jurkat) (n = 3, time: 8 days, one-way ANOVA with Dunnett’s multiple comparisons test). (E) Knockdown of PSIP1 in Jurkat reduces maximal respiration in a Seahorse XF Cell Mito Stress test (n = 9 technical replicates, one-way ANOVA with Dunnett’s multiple comparisons test). Oxygen consumption rate (OCR) with the sequential injections of oligomycin A, carbonyl cyanide p-trifluoromethoxyphenylhydrazone, and antimycin A + rotenone (left) and the maximal respiration plotted separately (right). *P < 0.05, ***P < 0.001, and ****P < 0.0001.