〔Abstract〕 Objective To study the effect of long non-coding RNA prostate cancer-associated transcript 1(lncRNA PCAT-1) on the proliferation and apoptosis of pancreatic cancer cells, and to explore its mechanism. Methods The expression level of lncRNA PCAT-1 in pancreatic cancer cell lines Capan-1,Capan-2, PANC-1,SW1990 and normal pancreatic cell hTERT-HPNE was detected by qRT-PCR. The highest lncRNA PCAT-1 expressing pancreatic cancer cell line was divided into sh-NC group and sh-PCAT-1 group. NC interfering with lentivirus(shRNA) and PCAT-1 shRNA infection were performed, qRT-PCR was used to detect the expression level of lncRNA PCAT-1 in each group of cells. [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2 H-tetrazolium, MTS] test was used to detect the effect of silenced lncRNA PCAT-1 expression on cell proliferation, flow cytometry was used to detect the effect of silenced lncRNA PCAT-1 on cell cycle and apoptosis, subcutaneous transplantation tumor test was used to detect the effects of silenced lncRNA PCAT-1 expression on pancreatic cell growthin vivo. Western blot was used to detect the effects of lncRNA PCAT-1 on the expression of cell cycle-related proteins, apoptosis-related proteins and key proteins of the PI3 K/AKT signaling pathway. Results qRT-PCR results showed that the expression level of lncRNA PCAT-1 in pancreatic cancer cell lines was higher than that in normal pancreatic cells hTERT-HPNE(P<0.05). Compared with Capan-1, Capan-2 and SW1990 cells, the expression of lncRNA PCAT-1 was the highest in PANC-1 cells, and the highest expression of lncRNA PCAT-1 was in PANC-1 cells. PANC-1 cells were infected with PCAT-1 shRNA, and qRT-PCR results showed that compared with the sh-NC group, the expression of lncRNA PCAT-1 in the cells of the sh-PCAT-1 group reduced(P<0.05); after silenced the lncRNA PCAT-1 expression in PANC-1 cells, cell proliferation ability reduced, cell cycle was arrested at G0/G1 phase, the apoptosis increased, tumorigenicity reduced in nude mice, cyclinD1 and CDK6 proteins expression decreased, and anti-apoptotic protein Bcl-2 expression decreased, the pro-apoptotic protein Bax expression increased, and the key proteins of PI3 K/AKT signaling pathway pPI3 K and pPAKT expression decreased. Conclusion Silencing the expression of lncRNA PCAT-1 may inhibit the proliferation and promote apoptosis of pancreatic cancer cells by regulating the PI3 K/AKT signaling pathway. lncRNA PCAT-1 may be a new target for the treatment of pancreatic cancer.