Fig. 1: PFTK1 was highly expressed in gefitinib-resistant NSCLC.

a, b HCC827 and PC9 cells were treated with a stepwise dose escalation of gefitinib (ranging from 0.1 to 5 μM) over for 1 year to establish resistant cell lines HCC827/GR and PC9/GR. Cell viability assays were performed in parental and resistant cells. The IC50 values of each cell to gefitinib were evaluated (n = 3). **p < 0.01. c The mRNA levels of the top 10 differentially expressed genes in Wnt signaling pathway from Gene Expression Microarray analysis were determined by qRT-PCR assays (n = 3). **p < 0.01. d WB assays and densitometric analysis for the expression of PFTK1 were conducted in the mentioned cells (n = 3). **p < 0.01. e HCC827 and PC9 cells were treated with 1 μM gefitinib for 0 h, 6 h, 12 h, 24 h, and 48 h, respectively. The PFTK1 expression levels were measured via qRT-PCR assays (n = 3). f The subcellular location of PFTK1 was estimated in NSCLC cells via IF assays. The staining intensity of the nucleus and the cytoplasm were quantified by Image J software (n = 3). Scale bars: 40 μm. g Six pairs of sensitive and gefitinib-resistant NSCLC tissues were collected and detected for PFTK1 expression by qRT-PCR assays (n = 3). h The PFTK1 expression levels were measured in another cohort of 67 cases of NSCLC tissues with gefitinib treatment via IHC assays. Based on PFTK1 expression, the patients were divided into two groups. Kaplan–Meier analysis was performed to evaluate the relationship between PFTK1 expression and the PFS of these patients. **p < 0.01.