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. 2024 Jun 15;15:5115. doi: 10.1038/s41467-024-49298-7

Fig. 3. Validation of ACSL3/G6PD synthetic lethality.

Fig. 3

A–C sgRNA-mediated depletion of ACSL3 causes reduced viability of NF2-KO cells but not NF2-WT cells. (A) Relative cell number 4 days after seeding (7 days post infection), assessed by CellTiter-Glo. Bars = mean ± SD. (B) Cell toxicity analyzed with CellTox. Values are normalized to total cell number (CellTiter-Glo). Bars = mean ± SD. C Representative control immunoblots to assess ACSL3 knock-out efficiency. A–B Significance by two-way ANOVA and Sidak’s multiple comparisons test. n = 5 (A) or 3 (B) biological replicates. D–E Induction of ACSL3 knockdown with two different shRNAs impairs viability of NF2 KO cells. D Immunoblot control of ACSL3 knockdown upon Dox treatment (1 µg/mL for 24 hrs) of human Schwann cell lines stably transfected to carry indicated shRNAs. E Relative cell number 4 days after induction (1 μg/ml doxycycline) of control or ACSL3 shRNA, each compared to non-induced controls (DMSO). Bars = mean ± SD. Significance by one-way ANOVA and Dunnett’s multiple comparisons test. n = 4 biological replicates. F ACSL3 knockdown reduces growth of NF2-KO Schwann cell tumor xenografts. Tumor volume as a function of time of NSG mice injected subcutaneously with indicated Schwann cell lines and treated +/- Dox for 25 weeks. Animals were randomized into the +dox vs -dox groups. Graphs show mean volumes; error bars=SEM. Significance by multiple unpaired t-test comparison analysis. Source data are provided as a Source Data file.