miR-203提高白血病K562细胞对熊果酸的敏感性研究

摘要

Aim To study the influences of miR-203 on ursolic acid (UA ) sensitivity in leukemic K562 cell.Methods In the experimental system,eukaryot-ic expression vector of hsa-miR-203 (PmiR-203 )was transfected into K562 cells using LipofectamineTM 2000.K562 cells were incubated with different con-centration of UA alone or in combination with PmiR-203 .The cell proliferation was analyzed by MTT as-say.The cell apoptosis was measured by double stai-ning with Annexin V and Propidium Iodide.The ex-pression of Bcr/abl protein was detected by Western Blot.Results The miR-203 promoted the sensitivity of UA by up to 1 .55-fold and the IC50 was reduced from 44.3μmol · L-1 to 30.7 μmol · L-1 .The a-mount of apoptotic cells was increased in UA combined with PmiR-203 group (P<0.05).PmiR-203 downreg-ulated the expression of Bcr/abl protein in K562 cells. Conclusion Our results support a substantial role of miR-203 that enhances UA sensitivity in K562 cell and the mechanism appears to be related to the dounregula-tion of Bcr/abl by miR-203 .%目的：研究miR-203影响白血病K562细胞对熊果酸的敏感性及可能的作用机制。方法利用脂质体 Lipo-fectamineTM 2000将miR-203的真核表达载体PmiR-203转染K562细胞。MTT法检测单纯使用PmiR-203、熊果酸以及两者联合使用对细胞的增殖抑制作用；Annexin V／PI双染法检测细胞早期凋亡率；Western blot检测细胞内bcr／abl蛋白表达水平。结果熊果酸与PmiR-203联合使用后，IC50从44.3μmol·L－1降低到30.7μmol·L－1，敏感性提高到单纯使用熊果酸的1．55倍。PmiR-203联合熊果酸组细胞早期凋亡率明显增加（P＜0.05）。PmiR-203组细胞内bcr／abl的表达水平明显降低。结论 PmiR-203可通过抑制Bcr／abl融合基因的表达发挥抗白血病作用，与熊果酸联合使用可提高白血病K562细胞对熊果酸的敏感性。