Fig. 5: Scaf1 regulates TNFa and p53 signaling as well as hedgehog signaling in response to Olaparib.
From: In vivo CRISPR screens reveal SCAF1 and USP15 as drivers of pancreatic cancer
A Volcano Blot showing differential expressed genes between Scaf1-knockout compared to control KC cells. Wald test and Benjamini-Hochberg (BH)-adjusted P-value. Two independent sgRNAs, two biological duplicates. B Bar graph showing gene set enrichment analysis of Scaf1-knockout compared to control KC cells. GSEA nominal p-values. Two independent sgRNAs, two biological duplicates. C Bar graph showing gene set enrichment analysis of Usp15-knockout and Scaf1-knockout compared to sgCtrl control KC cells treated with Olaparib (1 µM). GSEA nominal p-values. Two independent sgRNAs, two biological duplicates. D Expression levels of genes related to HH signaling evaluated by RT-qPCR in the indicated KC cell lines. Results were normalized with Gapdh and are expressed in fold change to CTRL (mean ± SEM, n = 3 independent experiments). Cells were treated with 100 nM Smoothened Agonist (SAG) and 1 µM Olaparib. Two-sided T-test, for sgUSP15: NRP2 p = 0.021/p = 0.018; PTCH1 p = 0.037/p = 0.033; GLI1 p = 0.033; NRP2 p = 0.042/p = 0.037; for sgScaf1: PTCH1 p = 0.046; PTCH2 p = 0.040/p = 0.042/p = 0.033; GLI1 p = 0.037/p = 0.031; NRP2 p = 0.042.
