Plantamajoside modulates the proliferation, stemness, and apoptosis of lung carcinoma via restraining p38MAPK and AKT phosphorylation

Lung cancer is the leading global cause of cancer-related mortality, with non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) accounting for roughly 85% and 15% of all incidence, respectively (1). At the time of diagnosis, most patients are already at a late stage of the disease, resulting in a high rate of mortality. Nowadays, new therapeutics like EGFR (epidermal growth factor receptor) inhibitors and immunotherapy offer benefit for lung cancer patients; nevertheless, the 5-year survival rate for patients is less than 20% (2,3). Some signal transduction pathways have been involved in the development of new lung cancer drugs, among which the VEGF, p38 MAPK, and PI3K signaling pathways have proved most attractive. The pathology of NSCLC is usually more closely related to p38 MAPK signaling, while the pathology of SCLC is more closely related to PI3K (4). The need for proper subclassification-based administration is becoming more urgent, and more targeted therapies desperately need to be developed (5)