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Fig. 2 | Molecular Cancer

Fig. 2

From: Reprogramming anchorage dependency by adherent-to-suspension transition promotes metastatic dissemination

Fig. 2

AST factor-mediated YAP-TEAD suppression dissociates cell–matrix interaction. A Immunofluorescence analysis of nuclear expression of ectopic V5-tagged 4 AST factors in HEK293A-4AST cells. Scale bar, 20 μm. B-D GSEA and heatmap of focal adhesion- and ECM-related genes in HEK293A-4AST cells compared to control cells. E–F Effect of restoring ECM (E, fibronectin) and focal adhesions (F, green, V5; red, vinculin) in doxycycline-induced HEK293A-ASTTetR cells. Scale bar 50 μm (E), 10 μm (F), Upper images; z-section, scale bar, 5 μm (F). G Immunoblotting analysis of AST factor-induced phosphorylation and inhibition of YAP. H Quantitative real-time PCR analysis of the TEAD2 transcript levels in 4 AST cells. I Analysis of H3K27ac ChIP-seq profiles at TEAD2 locus in HEK293A-mock and AST cells. J Analysis of H3K27ac ChIP-seq signal at the 4AST LOSS region in AST cells. Mean values are shown with error bars representing the s.d. of n = 3 independent replicates. *p < 0.05. K List of the top ten known motifs enriched at AST LOSS regions (n = 425). L Representative images of partial AST induction in TEAD KO cells cultured in low stiffness plates (40 kPa or 10 kPa). Scale bar, 50 μm. M Restoration of anchorage dependency in AST cells by ectopic expression of TEAD2 and constitutively active YAP-S127A. Scale bar, 50 μm. N–O Restoration of focal adhesion- and ECM-related gene signatures in HEK293A-4AST cells by reconstitution of TEAD2 and constitutively active YAP-S127A

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