Objective: To explore the influence of Imatinib on multiple myeloma cells expressing c-kit in vitro and its mechanism.
Methods: KM3 cells were treated with Imatinib at different concentrations, and cell growth index were evaluated by XTT assay, cell cycle by flow cytometry, apoptosis by Annexin V/ PI and DNA ladder, and change in protein level by Western blot.
Results: Imatinib inhibited proliferation of KM3 cells at concentrations more than 0.25 micromol/L in a dose-dependent manner, and the 48 h IC50 was 0.33 micromol/L (P < 0.01). Imatinib arrested cell in C0/G1 phase. Annexin V/PI staining and DNA ladder indicated that Imatinib had a substantial effect on inducing apoptosis of KM3 cells in a dose-dependent manner and induced pro-caspase-3 and poly ADP-ribose polymerase (PARP) cleaved. Imatinib inhibited expression of c-kit and provoked a decrease of IL-6 induced c-kit phosphorylation in vitro.
Conclusion: Imatinib inhibits KM3 cells proliferation and induces the cells apoptosis by inhibiting c-kit signalling transduction.