| Objective The study aimed to make clear the relationship betweenMyD88and the resistance of ovarian cancer cell to paclitaxel.Methods After knocking-down and over-expressing MyD88inA2780/Taxol cell line, qRT-PCR and western blot were performed totest the expression change of MyD88on mRNA and protein levelcompared with control group, respectively. CCK-8assay was executedto detect the change of resistance to paclitaxel in A2780/Taxol cells.The expression of pAkt, XIAP, MDR1was detected by WesternBlot.Flow cytometry was performed to test the affection to Cell cycleand apoptosis of A2780/Taxol cell line.Results By means of inhibiting MyD88, we observed that resistanceof A2780/Taxol to paclitaxel declined obviously, and anti-apoptoticsignificantly weakened. Further, inhibition of PKB/Akt signal pathwayor knock down of MDR1also can decrease the paclitaxel-resistance ofthe cells. Inversely, over-expression of MyD88increased cellsresistance to paclitaxel. Conclusion Down-regulation of MyD88increased sensitivity ofovarian cancer cell to paclitaxel, which provide new ideas and targets ofgene therapy for the clinical treatment of ovarian cancer resistantpatients. |
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