Fig. 2

KS cells enclose/hold the metabolic enzymes induction triggered by the single lesions. a Venn diagram of the unique and shared identified proteins among the NSCLC NCI-H1299 isogenic clones harbouring WT, K, S and KS genetic determinants. b Heat-map display of unsupervised hierarchical clustering of the relative intensity (log2) of the identified proteins. c Principal component analysis (PCA) using the identified proteins. d Unsupervised hierarchical clustering of the fold change in abundance of metabolic enzymes identified by label Free-SRM targeted proteomics in NSCLC NCI-H1299 isogenic clones. e Fold change in abundance of the significantly altered metabolic enzymes detected through SRM label free analysis in NSCLC NCI-H1299 harbouring KS, K and S relative to WT clone. f Fold change in abundance of the significantly altered metabolic enzymes detected through SRM label free analysis in NSCLC NCI-H1299 harbouring KS relative to K or S clone. Columns represent protein fold change in abundance (mean ± SD, 3 biological replicates). Red highlighted the most affected metabolic pathways based on both the number of significantly deregulated proteins relative to the number of overall monitored proteins by SRM target proteomic strategy and on the fold change of abundance (± two-fold changes). Statistical analysis was performed using two-way ANOVA and Mann-Whitney-Wilcoxon Test *p-value< 0.05, ***p-value< 0.001