Fig. 1: CMPK2 expression was associated with Osimertinib resistance in lung cancer cells independent of additional EGFR kinase domain mutations. | npj Precision Oncology

Fig. 1: CMPK2 expression was associated with Osimertinib resistance in lung cancer cells independent of additional EGFR kinase domain mutations.

From: Restoration of Osimertinib sensitivity in lung cancer through BRD4 inhibitor-mediated depalmitoylation of mutant EGFR via APT1

Fig. 1

PC-9 and PC-9/OR were treated with different concentrations of Osimertinib (0, 5, 10, 20, or 40 nM), and then A cell viability was determined by CCK-8 assay; B the expression of CMPK2 was measured by qRT-PCR; C the expression of CMPK2 and EGFR was measured by western blot; D immunofluorescence staining of EGFR (green) and nuclei (DAPI, blue). Red arrows indicated representative cells with prominent nuclear EGFR accumulation. Nuclear EGFR fluorescence intensity was quantified using ImageJ (scale bar = 25 μm). E, F The viability and proliferation of PC-9/OR cells were detected by CCK-8 and colony formation after silencing CMPK2 alone or simultaneously silencing CMPK2 and treating with Osimertinib. G, H The expression of CMPK2 and EGFR was examined by qRT-PCR and western blot in PC-9/OR cells silenced CMPK2 alone or simultaneously silenced CMPK2 and treated with Osimertinib. Mean ± SD, n = 3, *p < 0.05, **p < 0.01, ***p < 0.001. Statistical analysis was carried out by one-way ANOVA. CMPK2 cytidine monophosphate kinase 2, EGFR epidermal growth factor receptor, CCK-8 cell counting kit-8, qRT-PCR quantitative real-time polymerase chain reaction, PC-9/OR Osimertinib-resistant PC-9 cells.

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