Abstract: ObjectiveTo explore the effect of microRNA216 （miR-216） on the proliferation and apoptosis of pancreatic cancer cells and the drug resistance to gemcitabine. 
MethodsThe realtime quantitative PCR （QPCR） method was used to detect the miR216 level in the gemcitabine resistant cell line BxPC3 and the nondrugresistant cell line CFPAC1 of pancreatic cancer. The miR216 mimics （mimics group） and inhibitor （inhibitor group） were transfected to BxPC3 cells by Lipofectamine 2000 liposome method. BxPC3 cells transfected with liposomes were used as the control group. QPCR was used to detect the level of miR216 at 48 h after transfection. The CCK8 method was used to detect the absorbance of each group at 24， 48， and 72 h after transfection to evaluate the proliferation rate. Annexin ⅤFITC／PI double staining was used to detect the apoptotic rates of each group at 48 h after transfection. The CCK8 method was used to detect the half inhibitory concentration （IC50） of gemcitabine. The target gene of miR216 was predicted by bioinformatics database miRBase and Gene Oncology （GO） function was annotated by cytoscape 351 and its plugin CluGO. 
ResultsThe results of QPCR detection showed that the level of miR216 in BxPC3 cells was 3010±0901， higher than 1049±0074 of CFPAC1 cells （P＜0.05）. The expression levels of miR216 in the control group， mimics group and inhibitor group were 1130±0.145， 4.843±0.782 and 0.256±0145（P＜0.05）. Compared with the control group， the proliferative rates increased and apoptotic rates decreased in mimics group while the proliferative rates decreased and apoptotic rates increased in inhibitor group （P＜0.05）. The IC50 of gemcitabine were （2.134±0.591）μg／ml， （4.518±0.862）μg／ml and （0481±0073）μg／ml in the control group， mimics group and inhibitor group. The resistance of BxPC3 cells to gemcitabine decreased after transfection of miR216inhibitor， and the resistance to gemcitabine increased after transfection of miR216mimics （P＜0.05）. There were 138 predicted target genes of miR-216. GO functions are mainly enriched in proliferation， apoptosis， invasion and migration. 
ConclusionThe expression of miR216 is upregulated in pancreatic cancer drug resistant cells and can induce the proliferation of cancer cells， suggesting that it can play a similar role in promoting tumor genes and participate in the process of gemcitabine resistance， and it may become a target for early diagnosis and new biological treatment of pancreatic cancer.

Key words: Pancreatic cancer, MicroRNA216, Gemcitabine, Proliferation