Fig. 4: The gene regulatory network of cancer cells following activation of the Hippo pathway. | Communications Biology

Fig. 4: The gene regulatory network of cancer cells following activation of the Hippo pathway.

From: Genome-wide CRISPR screens identify the YAP/TEAD axis as a driver of persister cells in EGFR mutant lung cancer

Fig. 4

a Transcription factor (TF) activity following activation of Hippo signaling through NF2 loss or overexpression of WWTR1 or YAP1 in EGFR mutant lung cancer cells. Cut-off for TF selection was p < 0.01 after enrichment using Enrichr. Heatmaps show inferred TF activity (log2 normalised). Scales are normalised to maximum and minimum of each heatmaps. b–e STRING interaction networks of activated TFs following (i) NF2 loss, (ii) overexpression of WWTR1 or YAP1, or (iii) osimertinib treatment in PC-9, HCC827 and HCC4006 cancer cells (160 nM for 48 h). The mean activity score for each TF is indicated by the colour intensity of each box and the bars within each box represent individual elements that comprise that mean score. Number of deregulated genes (cut-off p < 0.01, FC + /−1.5) after Hippo effector upregulation cause and enrichment of Hallmark pathways in (f) PC-9, (g) HCC827, and (h) HCC4006 cells. Cut-off for pathway selection was p < 0.01 after enrichment. Graphs show Enrichr score as a combined measure of significant enrichment and signature size.

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