目的：探讨在子宫内膜癌细胞中重组人程序性细胞死亡蛋白5 （recombinant human programmed cell death protein 5，rhPDCD5）对紫杉醇化疗的促进作用。 方法： 子宫内膜癌KLE细胞培养完成后，通过重组人rhPDCD5 （20 μg/ml）处理KLE细胞，再分别以0、1.0、5.0、10.0、50 μmol/L紫杉醇（paclitaxel, PTX）处理24 h或以10 μmol/L PTX 处理0、12、24、48 h，提取细胞总RNA及蛋白后，CCK法检测KLE细胞的增殖情况，流式细胞术检测KLE细胞凋亡情况，实时定量PCR检测KLE细胞中PDCD5 mRNA的表达量，实时定量PCR或Western blotting测定凋亡相关基因的Bax、Bcl2、caspase-3 mRNA或蛋白水平的变化。 结果：PTX对PDCD5表达的促进作用具有剂量依赖性和时间依赖性；PTX的最佳作用浓度为10 μmol/L，最佳作用时间为24 h。rhP-DCD5明显增强紫杉醇对KLE细胞的抑制作用。CCK实验、流式细胞术及Western blotting检测显示：PTX+rhPDCD5联合处理组KLE细胞的增殖抑制率和凋亡率均较PTX组明显增加、pro-caspase 3的表达量明显增加（均P<0.01）。促进凋亡蛋白Bax和抑制凋亡蛋白Bcl2的比值亦较明显增加（P<0.01）。 结论： rhPDCD5可协同PTX抑制子宫内膜癌KLE细胞的增殖、促进细胞的凋亡，可明显增强KLE细胞对PTX的药物敏感性。

Objective:To explore the promoting effect of rhPDCD5 (recombinant human programmed cell death protein 5) on paclitaxel (PTX) chemotherapy in endometrial carcinoma cells. Methods: After routine culture, endo-metrial carcinoma KLE cells were treated with rhPDCD5 (20 μg/ml), and then treated with PTX at different concen-trations (0, 1.0, 5.0, 10.0 and 50 μmol/L) for 24 hours or 10 μmol/L PTX for different time periods (0，12，24，48 h).The proliferation of KLE cells was determined by CCK, the apoptosis was examined by Flow cytometry, the PDCD5 mRNA was determined by Real-time quantitative (qPCR), and the changes of apoptosis-related genes (Bax,Bcl2, caspase 3) at protein and mRNA level were detected by western blotting and q-PCR, respectively. Results:The promoting effect of PTX on PDCD5 expression was dose- and time- dependent. The optimal concentration of PTX was 10 μmol/L and the best treatment duration was 24 hours. rhPDCD5 significantly promoted the inhibitory effect of PTX on KLE cells. CCK-8 assay and Flow cytometry confirmed that the proliferation inhibitory rate and apoptosis rate were significantly enhanced in PTX+rhPDCD5 group, compared with PTX group (P<0.01); In the presence of PTX and rhPDCD5, the expression level of pro-caspase 3 was significantly increased (P<0.01); more-over, the ratio of Bax to Bcl2 was significantly higher in PTX+rhPDCD5 group than that in other groups (P<0.01).Conclusion: rhPDCD5 can enhance the inhibitory effect of PTX on proliferation of KLE cells, promote cell apopto-sis and significantly enhance the PTX susceptibility of KLE cells.