To explore the molecular mechanism of phosphatidylinositol 3-kinase/protein kinase B signaling pathway（PI3K/Akt signaling pathway）affecting the sensitivity of human pancreatic cancer cell line（PANC-1）to gemcitabine chemotherapy.

Flow cytometry was used to detect the effect of PI3K/Akt signaling pathway inhibitor LY294002 combined with gemcitabine on PANC-1 cell apoptosis. RNA interference was used to silence Paul-like kinase 1（Plk1）gene（shPlk1），and flow cytometry was used to detect the effect of gemcitabine on PANC-1 cell apoptosis after Plk1 downregulation. PANC-1 cells were treated with LY294002，and the levels of phosphorylated protein kinase B（p-Akt）and Plk1 were detected by Western blot assay. PANC-1 cells were treated with shPlk1 and the protein levels of Plk1 and p-Akt were detected by Western blot. The statistical software of GraphPad InStat3 and SPSS21.0 was used for analysis. Data were expressed as（

LY294002 could promote the sensitivity of PANC-1 cells to gemcitabine（P<0.01）. Down-regulating Plk1 significantly increased the sensitivity of PANC-1 cells to gemcitabine（P<0.01）. Compared with blank group（no treatment），the protein expression levels of P-Akt and Plk1 in LY294002 treatment group were significantly decreased（P<0.01）. Compared with blank group，the protein level of Plk1 in shPlk1 treatment group was significantly decreased（P<0.01），while the protein level of P-Akt in ShPLK1 treatment group was not significantly changed（Ｐ>0.05）.

PI3K/Akt signaling pathway is closely related to gemcitabine chemotherapy sensitivity of pancreatic cancer cells，and inhibition of PI3K/Akt signaling pathway promotes gemcitabine chemotherapy sensitivity of pancreatic cancer cells by down-regulating Plk1 protein.