Fig. 1: Hyperactivated EGFR signaling promotes resistance to cisplatin, leading to poor survival in cervical cancer patients.
a Kaplan–Meier analysis of overall survival (calculated as months to death or months to last follow-up) in cisplatin-treated CESC or cisplatin-untreated CESC. The 30th and 70th percentiles were used as cutoffs values for the EGFR activity scores (EGFR activity scorehigh > 70th; EGFR activity scorelow < 30th). b Comparison of the level of EGFR activity scores in responder (R, n = 55) and non-responder (NR, n = 12) of cisplatin-treated CESC cohort. c Western blot analysis of pEGFR, EGFR and MCL1 expression. d, e CaSki P and CR cells were treated with gefitinib as the indicated dose. f, g CaSki P and CR cells were transfected with siRNA targeting GFP or EGFR. d, f The protein levels of pEGFR, EGFR and MCL1 were determined by western blots. β-actin was used as an internal loading control. Numbers below the blot images indicate the expression as measured by fold-change. e, g Flow cytometry analysis of the frequency of apoptotic (active caspase 3+) cells after incubation with or without cisplatin for 24 h. All experiments were performed in triplicate. In the box plots, the top and bottom edges of boxes indicate the first and third quartiles, respectively; the center lines indicate the medians; and the ends of whiskers indicate the maximum and minimum values, respectively. The p values by Gehan–Breslow–Wilcoxon test (a), two-tailed Student’s t test (b) or two-way ANOVA (e, g) are indicated. The data represent the mean ± SD. Source data are provided as a Source Data file.
