Delicaflavone induces apoptosis and autophagy, and improves the cytotoxicity of multiple myeloma cells to cisplatin by inactivating the AKT/mTOR pathway

Abstract


 
 
 
 Purpose: To determine the effects of delicaflavone in multiple myeloma cells.
 Methods: Multiple myeloma cells were incubated with different concentrations of delicaflavone (20, 40, and 80 μM) or coincubated with 40 μM delicaflavone and 20 μM cisplatin. Cell viability and proliferation were investigated using MTT and colony formation assays, respectively. Flow cytometry and western blot analysis were applied to investigate cell apoptosis and autophagy.
 Results: Treatment with delicaflavone decreased cell viability and proliferation of multiple myeloma cells but promoted cell apoptosis in a dose-dependent manner. Protein expression of Autophagy-related protein 7 (Atg7) and LC3-II/LC3-I were increased by delicaflavone treatment, while p62 was decreased by the same treatment. Delicaflavone also conferred cisplatin sensitivity in multiple myeloma cells through decreases in cell viability and in cell proliferation. AKT/mTOR phosphorylation was reduced in multiple myeloma cells treated with delicaflavone.
 Conclusion: Delicaflavone induces apoptosis and autophagy of multiple myeloma cells, and confers cisplatin sensitivity through inactivation of the AKT/mTOR pathway.
 
 
 

Expression of mTOR conduction pathway in human osteosarcoma MG-63 cells and their stem cells, and the inhibitory effect of different doses of rapamycin

“…It plays a role as the central regulatory point in the process of tumor cell differentiation, growth, and proliferation. Rapamycin specifically binds to the mTOR protein to effectively block the cell mTOR function, and also has an anti-tumor biological effect [11][12][13]. Studies have shown that ap2357, a derivative of rapamycin, can have a good effect on soft tissue tumors and malignant bone tumors, and inhibits the proliferation of sarcoma cells in intimal cells in vitro.…”