Chen Yu,Deng Zhongliang.Effect of protein kinase C on multidrug resistance in human osteosarcoma cells and its underlying mechanism[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(18):1900-1903.
Chen Yu,Deng Zhongliang.Effect of protein kinase C on multidrug resistance in human osteosarcoma cells and its underlying mechanism[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(18):1900-1903.DOI:
Effect of protein kinase C on multidrug resistance in human osteosarcoma cells and its underlying mechanism
Objective To study the expression of major protein kinase C (PKC) subtypes in human osteosarcoma 143B cells and its relation with drug resistance to 143B cells. Methods Expression levels of p-PKCα
p-PKCβ
p-PKCγ and multidrug resistance protein 1 (MDR-1) in wild human osteosarcoma cells or 143B/ADM-drug resistant cells were measured by Western blotting. Effect of PKC on expression of MDR-1 was inhibited by the PKC special inhibitor
staurosporine. Drug sensitivity was measured by CCK assay. Concentration of adriamycin (ADM) in 143B cells was measured by fluorescence spectrometry. Cell apoptosis and extracellular rho123 levels were measured by flow cytometry. Results The expression level of p-PKCα was significantly higher in 143B/ADM-drug resistant cells than in 143B/WT cells. However
no significant difference was found in expression of p-PKCβ and p-PKCγ. The expression of MDR-1 in 143B/ADM-drug resistant cells was significantly up-regulated. The drug-resistant index to ADM was 15.7 in 143B/ADM-drug resistant cells but decreased to 5.5 after the expression of PKC in 143B/ADM cells was inhibited by staurosporine (P0.01). The apoptosis rate of 143B/ADM-drug resistant cells was 28.41%±4.33% and increased to 70.63%±4.80%
while the extracellular rho123 level and MDR-1 expression level were significantly down-regulated after the expression of PKC in 143B/ADM cells was inhibited by staurosporine (P0.01). Conclusion Over-expression of PKCα in drug-resistant human osteosarcoma 143B cells may attenuate drug resistance by regulating MDR-1 expression.