Fig. 3: Serine-mediated carboplatin resistance is regulated by ΔNp63α in LUSC.

The TCGA Firehose Legacy dataset on the cBioPortal platform was used to analyze TP63 gene alterations (A) and mRNA expression (B) in LUAD and LUSC. C The “Hou Lung dataset” from the Oncomine database was used to analyze the Pearson correlation coefficient (R value) and a two-tailed probability test (p-value) between the mRNA levels of TP63 and serine synthesis enzymes. D Whole cell lysates derived from NCI-H1703, NCI-H520, HCC95 cells, and HEK-293T cells transiently transfected with TAp63α, ΔNp63α, ΔNp63β, or ΔNp63γ were subjected to immunoblot analysis. NCI-H520 cells stably expressing ΔNp63α (WT and R304W) were subjected to immunoblot analysis (E) and measurement for cellular serine level (F). NCI-H1703 and HCC95 cells stably expressing a control shRNA (shC) or two different shRNAs specific for p63 were subjected to immunoblot analysis (G) and measurement for cellular serine level (H). I, J NCI-H520 cells stably expressing empty vector (EV) or ΔNp63α were grown in media with or without serine (-S), without serine and glycine (-SG), and treated with or without carboplatin for 48 h, then subjected to CCK-8 assay for cell viability, measurement for GSH and formate levels (I), and immunoblot analysis for γH2AX level (J). *p < 0.05; **p < 0.01; NS not significant.