Fig. 1: PLK1 inhibitors exhibit broad-spectrum antiproliferative activity and clinical potential for EGFR-mutant NSCLC.

A Screening of compound library was performed to assess the anti-proliferation activity in PC9 and NCI-H1975 cells at a concentration of 100 nM for 5 days. B IC₅₀ values of PLK1 inhibitors and EGFR-TKIs were measured in EGFR-mutant NSCLC and Ba/F3 cell lines with different EGFR mutations following treatment for 5 days. C The volcano plot analysis of the differential gene expression in PC9 cells following treatment with 40 nM volasertib for 24 h, as compared to control (|Log2FC|> 0 and P < 0.05). D KEGG enrichment analysis of downregulated genes by volasertib (Log2FC < 0 and P < 0.05). E Relative PLK1 mRNA expression in tumor tissues was compared to adjacent normal tissues from EGFR-mutant NSCLC patients, as assessed using the Wilcoxon test (***P < 0.001). F Gene expression data of EGFR-mutant NSCLC patients (n = 80) from the TCGA database were utilized for conducting gene set enrichment analysis (GSEA) on PLK1 gene (NES > 1, FDR < 0.05). G GSEA analysis of the correlation between the PLK1 gene and ErbB signaling pathway in EGFR-mutant NSCLC patients. H A mutation information matrix of genes associated with the ErbB signaling pathway was constructed for NSCLC patients harboring EGFR mutations and stratified by high or low PLK1 mRNA expression (n = 80). I Cumulative mutations of the ErbB signaling pathway genes were compared between high and low PLK1 expression groups, as assessed using a two-tailed unpaired Student’s t test (*P < 0.05). J Kaplan-Meier survival curves of EGFR-mutant NSCLC patients stratified by PLK1 expression after PSM to exclude the effects of stage.