LKB1-deficient NSCLC cells show vulnerability to high-dose AA-induced pyroptosis.

The deficiency of LKB1 in tumor cells impairs their ability to sense metabolic stress appropriately,ultimately leading to redox imbalance. LKB1-deficient NSCLC cells predominantly take up ascorbic acid. Inflammatory PCD, including necroptosis, pyroptosis and PANoptosis, could release inflammatory mediators and switch the inflammatory state of TIME. Previous study demonstrated that high-dose AA could promote lung cancer cell death, but the modality of cell death still remained unclear. To further investigated the precise modality of the above inflammatory PCD, we performed RNA sequencing on cells with deficient or intact LKB1 pretreated with high-dose AA or not and then analyzed the established different forms of programmed cell death signaling gene. Gene expression profiling analysis of RNA-sequencing of A549 cells with deficient or intact LKB1 pretreated with or without high-dose AA, 3 replicates for each group.