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Archive > Volume 24 Issue 10 > 2017,24(10):1101-1106. DOI:10.3872/j.issn.1007-385X.2017.10.010 Prev Next
Clinical Research
rhPDCD5 enhances susceptibility of endometrial cancer KLE cells to paclitaxel
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Abstract:
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.
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