Flemiphilippinin A induces paraptosis in lung cancer cells via c-Myc-driven endoplasmic reticulum stress and CHOP-mediated mitochondrial dysfunction

This research demonstrates that Flp-A exerts potent anti-tumor effects against lung cancer by targeting c-Myc to induce excessive ER stress and mediating mitochondrial dysfunction through CHOP, ultimately triggering paraptosis. Furthermore, Flp-A increases sensitivity of lung carcinoma cells to gefitinib through paraptosis induction. Our work provides the first evidence for Flp-A's anti-lung cancer mechanism via the paraptosis pathway and confirms its safety profile. Additionally, we reveal Flp-A's capacity to bypass gefitinib resistance in lung carcinoma. These findings position Flp-A as a encouraging novel medical agent for lung cancer treatment, particularly for addressing drug resistance.