Fig. 3: HGF induces TWIST1 expression and EMT in NSCLC. | Oncogene

Fig. 3: HGF induces TWIST1 expression and EMT in NSCLC.

From: TWIST1 is a critical downstream target of the HGF/MET pathway and is required for MET driven acquired resistance in oncogene driven lung cancer

Fig. 3

A Induction of endogenous TWIST1 and additional EMT markers after HGF treatment in MET wild type Non-Squamous NSCLC cell lines (A) H23 (B) 11-18 (C) HCC-827 or exogenously expressed TWIST1 in D H460 cells. E HGF overexpression drive TWIST1 and E2A expression in murine NSCLC cells derived from carcinogen induce lung tumors in wild type FVB/N (FVBW-17) or transgenic mouse model with lung specific Hgf expression (FVB-HGF) respectively. F Microscopic images (20X) of FVBW-17 and FVB-HGF cells, phase-contrast (left) and fluorescence microscopy (right). The FVB-HGF cells have a more mesenchymal phenotype compared to FVBW-17 cells. G HGF treatment stabilizes TWIST1 through an ERK-dependent manner. H1993 cells overexpressing either wild type or S68D TWIST1 protein were treated with either an ERK inhibitor (LY3214996, 250 nM) or MET inhibitor (Capmatinib, 50 nM) and protein was collected at 48 h and western blot performed. H HGF regulates TWIST1 expression at the posttranslational level. HGF treatment increases the half-life of TWIST1 protein in H23 cell line. Protein concentration was quantified using densitometry and protein half-lives were determined using linear regression.

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