Fig. 5 | Nature Communications

Fig. 5

From: Functional linkage of gene fusions to cancer cell fitness assessed by pharmacological and CRISPR-Cas9 screening

Fig. 5

Therapeutically actionable oncogenic fusions identified across different histologies. a RAF1, NUTM1, and RSPO2/3 fusions identified in patients previously (left) and cell lines in this study (right). Cell lines with known oncogenic fusions used as positive controls are reported. b Interphase fluorescence in situ hybridization (FISH) of ATG7-RAF1 (left) and BRD4-NUTM1 (right) gene fusions (arrows) in PL18 and SBC-3 cell lines. The percentage of fusion-positive interphases are reported in white text. Schematic representations of each fusions are represented. Only exons involved in the breakpoint or displaying fusion mapping single guide RNA (sgRNAs) (red diamonds) or non-mapping sgRNAs (empty diamonds) are shown. c Fold change fusion essentiality score (FES) values of sgRNAs targeting ATG7 and RAF1 in PL18 (left) and BRD4 and NUTM1 in SBC-3 cells (right). Colored bars indicate values of sgRNAs targeting the exons involved in the fusions. d Depletion of fusion-targeting ATG7 guides for all screened pancreatic cancer cell lines. e Viability assay on PL18, SBC-3, EGI-1, and ESO51 cells treated with MEK (trametinib), BET (OTX-015), and PORCN (LGK974) inhibitors, respectively. SU8686, H196, and HCT116 cells are pancreatic, small-cell lung cancer, and colorectal cancer-negative controls. OCIAML2, RPMI2650, and SNU1411 are, respectively, a RAF1-rearranged leukemia, a NUTM1-rearranged NUT midline carcinoma (NMC), and a RSPO3-rearranged CRC cell line included as positive controls. Data are average ± s.d. of three technical replicates and are representative of three independent experiments

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