Objective       To investigate the mechanism of myeloid differentiation factor88 (MyD88) in the regulation of drug-resistance of human ovarian carcinoma A2780/Taxol cells.       Methods      The expression of MyD88 in A2780/Taxol cells was knocked down

by short interfering RNA (siRNA) of MyD88. Cell livability and proliferation in presence or absence of Taxol were detected by CCK-8 kit. The expression of p-Akt

X-linked inhibitor of apoptosis protein (XIAP)

multidrug resistance 1 (MDR1) was detected by Western blotting. After the PKB/Akt signal pathway was inhibited by LY294002 and the expression of MDR1 was knocked down by siRNA of MDR1

CCK-8 kit was used to detect the cell proliferation after Taxol treatment.       Results       The knock down of MyD88 in A2780/Taxol cells inhibited the cell proliferation (

P

0.05). The knock down of MyD88 in A2780/Taxol cells also decreased the paclitaxel-resistance of the cells and IC

50

was decreased to 50% of the control cells (

P

0.01). The increase of Akt

XIAP and MDR1 after paclitaxel treatment was also repressed by the down-regulation of MyD88. Further

inhibition of PKB/Akt signal pathway or knock down of MDR1 also can decrease the paclitaxel-resistance of the cells. The IC

50

was decreased to 80% and 50% of the control cells respectively (

P

0.05).       Conclusion      MyD88 promotes the drug-resistance of A2780/Taxol cells through regulating PKB/Akt signal pathway and MDR1 expression. MyD88 can be a new target for the clinical treatment of ovarian cancer resistance.