Fig. 2: Effects of PFTK1 involved in gefitinib resistance of NSCLC.

a HCC827 and PC9 cells were stably transfected with PFTK1 overexpression plasmid, b HCC827/GR and PC9/GR cells were transfected with shRNAs targeting PFTK1. a, b qRT-PCR and western blot analysis were conducted to measure the expression of PFTK1 in mentioned cells. Also, the densitometric analysis for the expression of PFTK1 was conducted in mentioned cells (n = 3). **p < 0.01. c, d Above cells were treated with gefitinib at the indicated concentration for 72 h, cell viability was evaluated by MTS assay (n = 3). **p < 0.01. e Cells (HCC827 and PC9 cells with restored PFTK1 and control group, HCC827/GR and PC9/GR cells with knocking down PFTK1 and control group) were seeded into a six-well plate, followed by 0.5 μM gefitinib treatment. Then, the cell clone numbers were estimated in each group (n = 3). **p < 0.01. f Cells were treated with 5 μM gefitinib for 72 h, and then the cell apoptosis was analyzed by flow cytometry (n = 3). **p < 0.01. g The workflow was showed. Tumor cells were cultured and subcutaneously inoculated into recipient nude mice. When the tumor volume was ~100 mm³, the mice were treated with gefitinib at a dose of 30 mg kg⁻¹, daily for 20 days. The elements of this image were created from icofont website (https://www.iconfont.cn). h HCC827/Luc cells with restored PFTK1 and vector, HCC827/GR/Luc cells with shRNA targeting PFTK1 and control, were subcutaneously injected into BALB/c nude mice to establish a xenograft tumor model. These mice were treated with gefitinib. Luciferase activity was imaged and measured by In Vivo Xtreme from Bruker (n = 3). “gefitinib” was abbreviated as “Gef”. **p < 0.01.