Supplementary Materials

The PDF file includes:

  • Text S1. Chemical synthesis details and methods.
  • Fig. S1. Genome-wide CRISPRi screening in the cancer cell line H358 identifies genes that influence cell growth and survival.
  • Fig. S2. Genome-wide CRISPRi screening in the cancer cell line MIA PaCa-2 identifies genes that influence cell growth and survival.
  • Fig. S3. FOSL1 minimally modulates p-ERK and p-S6 phosphorylation dynamics.
  • Fig. S4. Unique genetic dependencies within common signaling modules are revealed by evaluating ARS-1620 CRISPRi selection screens from distinct cancer cell lines.
  • Fig. S5. Cellular response to KRASG12C inhibition is mediated through phosphorylation changes in substrates of hit kinases.
  • Fig. S6. CDK4/6i coinhibition minimally alters p-AKT and p-ERK phosphorylation dynamics.
  • Fig. S7. EGFRi cotreatment enhances the suppression of oncogenic RAS signaling by ARS-1620 in vivo.
  • Table S1. sgRNAs used for individual retesting.
  • Legends for data file S1 to S5

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Other Supplementary Material for this manuscript includes the following:

  • Data file S1 (Microsoft Excel format). H358 ARS-1620 genome-wide CRISPRi sgRNA counts and phenotypes.
  • Data file S2 (Microsoft Excel format). H358 ARS-1620 genome-wide CRISPRi gene phenotypes.
  • Data file S3 (Microsoft Excel format). MIA PaCa-2 ARS-1620 genome-wide CRISPRi sgRNA counts and phenotypes.
  • Data file S4 (Microsoft Excel format). MIA PaCa-2 ARS-1620 genome-wide CRISPRi gene phenotypes.
  • Data file S5 (Microsoft Excel format). ARS-1620 global phosphoproteomics.