Objective： The aim of our study was to investigate the effect of bortezornib in combination with arsenic trioxide （As2O3） on the proliferation and apoptosis in the human multiple rnyelorna cell line KM3. Methods： ...Objective： The aim of our study was to investigate the effect of bortezornib in combination with arsenic trioxide （As2O3） on the proliferation and apoptosis in the human multiple rnyelorna cell line KM3. Methods： KM3 cells were cultured with different concentrations of bortezomib, As2O3 alone or in combination for different times. Cell proliferation was analyzed by MTT assay, and the ICso was calculated. Cell morphology was observed under the light microscope （using Wright-Giernsa stain） and electric microscope. Agarose gel electrophoresis was used to evaluate DNA content. Flow cytornetry was used to examine Annexin V-FITC/PI stain and mitochondrial transmembrane electric potential （△ψm）. Results： Bortezornib and As2O3 alone both inhibited KM3 cell proliferation in a time and dose dependent manner, with the IC50 were 0.27, 3.10 μmol/L, respectively; the inhibiting rate on KM3 cells of bortezornib plus As2O3 was significantly higher than bortezornib alone （18.22± 1.04）% vs. （13.18± 1.29）%, P 〈 0.05; A series of typical morphological features of apoptosis and a typical DNA ladder were observed in KM3 cell treated with 0.25 μm/L bortezornib for 48 h, which showed increased Annexin V positivity and decreased △ψm. The apoptosis rate induced by bortezornib plus As2O3 was also significantly than that of induced by bortezornib alone. Conclusion： Bortezornib could inhibit the proliferation while induce apoptosis of KM3 cells which may be through decreased △ψm. Bortezornib had enhanced inhibitory effect with As2O3 on the growth of KM3 cell （P 〈 0.05）. As2O3 enhances the apoptosis effects of bortezomib on KM3 cell.展开更多
文摘Objective： The aim of our study was to investigate the effect of bortezornib in combination with arsenic trioxide （As2O3） on the proliferation and apoptosis in the human multiple rnyelorna cell line KM3. Methods： KM3 cells were cultured with different concentrations of bortezomib, As2O3 alone or in combination for different times. Cell proliferation was analyzed by MTT assay, and the ICso was calculated. Cell morphology was observed under the light microscope （using Wright-Giernsa stain） and electric microscope. Agarose gel electrophoresis was used to evaluate DNA content. Flow cytornetry was used to examine Annexin V-FITC/PI stain and mitochondrial transmembrane electric potential （△ψm）. Results： Bortezornib and As2O3 alone both inhibited KM3 cell proliferation in a time and dose dependent manner, with the IC50 were 0.27, 3.10 μmol/L, respectively; the inhibiting rate on KM3 cells of bortezornib plus As2O3 was significantly higher than bortezornib alone （18.22± 1.04）% vs. （13.18± 1.29）%, P 〈 0.05; A series of typical morphological features of apoptosis and a typical DNA ladder were observed in KM3 cell treated with 0.25 μm/L bortezornib for 48 h, which showed increased Annexin V positivity and decreased △ψm. The apoptosis rate induced by bortezornib plus As2O3 was also significantly than that of induced by bortezornib alone. Conclusion： Bortezornib could inhibit the proliferation while induce apoptosis of KM3 cells which may be through decreased △ψm. Bortezornib had enhanced inhibitory effect with As2O3 on the growth of KM3 cell （P 〈 0.05）. As2O3 enhances the apoptosis effects of bortezomib on KM3 cell.
