Physalin B inhibits cell proliferation and induces apoptosis in undifferentiated human gastric cancer HGC‐27 cells

Abstract Background Physalin B (PB) from Physalis angulata L . (Solanaceae) is a naturally occurring secosteroid with multiple biological activities, including anti‐inflammatory and anticancer activity. However, PB's effects and mechanisms in human gastric cancer (GC) cells are not well characterized. Methods The undifferentiated GC cell line HGC‐27 and semi‐differentiated GC cell line SGC‐7901 were treated with PB. Cell counting kit‐8 (CCK‐8) and colony formation assays were performed to evaluate cell viability. Apoptosis and the cell cycle were assessed by Annexin V/PI and PI/RNase DNA staining assays, respectively, and Western blotting was used to evaluate the expression of a protein. Results PB significantly inhibited the proliferation of HGC‐27 cells in a dose‐ and time‐dependent manner. Moreover, PB induced G0/G1 cycle arrest and caspase‐dependent apoptosis of HGC‐27 cells. Cleaved caspases 8, 3, and 7, poly(ADP)‐ribose polymerase (PARP), and the cyclin‐dependent kinase (CDK) inhibitor p‐Chk2 was induced by PB in HGC‐27 cells, while the cell cycle‐related proteins cyclin D1, cyclin D3, CDK4, CDK6, cyclin E, and phosphorylated retinoblastoma tumor suppressor protein (p‐Rb) were downregulated in a dose‐dependent manner. Conclusions PB inhibits proliferation via cyclin‐dependent kinase and induces caspase‐dependent apoptosis in HGC‐27 cells, suggesting that PB might be a novel and effective agent for undifferentiated GC therapy.