Fig. 5: The effect of FMF targeting PFTK1 on gefitinib resistance in NSCLC.
a The 2D and 3D view of molecular docking was showed by MOE output. b–e HCC827/GR and PC9/GR cells were co-treated with FMF and gefitinib. The expression levels of PFTK1 (b), the cell colony-forming ability (c), the cell viability (d), and the cell apoptosis (e) were measured in each group (n = 3). **p < 0.01. f, g HCC827/GR and PC9/GR cells were treated with FMF, WB assays (f) and dual-luciferase reporter gene assays (g) were carried out to measure the activity of Wnt/β-catenin signaling pathway (n = 3). **p < 0.01. h Illustration for CDX development. The elements of this image were created from icofont website (https://www.iconfont.cn). HCC827/GR cells with luciferase were subcutaneously injected into nude mice. When tumor size reached 100 mm3, FMF and gefitinib were used daily to treat these nude mice by oral gavage for 20 days. Luciferase activity was imaged and measured by In Vivo Xtreme from Bruker (n = 3). **p < 0.01. i A schematic diagram depicts how PFTK1 upregulated by gefitinib actives Wnt/β-catenin signaling pathway to promote gefitinib resistance in NSCLC. We drew it on Figdraw (https://www.figdraw.com/).
