〔Abstract〕 Objective To investigate the role of CCL23 and CCR1 in human epithelial ovarian cancer cells cisplatin resistance. Methods The expression of CCL23 and CCR1 in human epithelial ovarian cancer cisplatin resistant cells C13 K and cisplatin sensitive cells OV2008 was detected by Real-time quantitative PCR(qRT-PCR). CCL23 over expression vector was constructed in OV2008 cells and the positive clones were selected by puromycin. The transfection efficiency was observed by fluorescence microscopy and qRT-PCR. After treated with BX471(CCR1 antagonist), cell proliferation and the half inhibitory concentration of cisplatin(IC50)were assessed by plate clone formation assay and CCK-8 assay respectively. The protein expression of CCL23, CCR1 and YAP(yes-associated protein) was detected by Western blot. Results qRT-PCR showed that the expression of CCL23 and CCR1 in C13 K cells was higher than that in OV2008 cells(P<0.01). Fluorescence microscopy showed that recombinant OV2008 cells were full of green fluorescence. The mRNA level of CCL23 in CCL23 overexpressing cells significantly increased(P<0.001) which proved that the CCL23 gene over expression of OV2008 cells was successfully constructed, but the mRNA level of CCR1 had no significant change(P>0.05). Plate clone formation assay and CCK-8 assay showed that the proliferation ability and cisplatin resistance of OV2008 cell line overexpressing CCL23 increased compared to the empty vector of OV2008 cell line and normal OV2008 cell line(P<0.01). BX471 inhibited the expression of CCL23 and CCR1, meanwhile, downregulated the expression of YAP. Cell proliferation was inhibited and cisplatin sensitivity increased after treated with BX471. Conclusion CCR1/CCL23 axis is involved in EOC cells cisplatin resistance and its mechanism may be related to the regulation of downstream effector YAP by CCL23 and CCR1.