Abstract:【Abstract】 Objective To investigate the mechanism of LncRNAANCR mediating the proliferation and migration of human gastric cancer cells by PI3K and AKT proteins.Methods Human gastric cancer cell lines were randomly divided into gastric cancer group (GC group), ANCR siRNA group (siRNA group) and LncRNA ANCR group (ANCR group). At the same time, normal gastric epithelial cells were selected as normal gastric cell group. GC group: simple gastric cancer cell line. siRNA group: ANCR siRNA was transfected into gastric cancer cells; ANCR group: LncRNA ANCR was transfected into gastric cancer cells. The proliferation, PI3K and AKT protein expression, apoptosis and invasive ability of gastric cancer cells in three groups were analyzed by TUNEL, Transwell, CCK 8, Western blot and RT-PCR. Differential expression of PI3K and AKT mRNA were explored the mechanism of LncRNA ANCR mediating PI3K and AKT protein on proliferation and migration of human gastric cancer cells.Results Transwell invasion experiments were performed on three groups of gastric cancer cells. It is obvious that the gastric cancer cells in the ANCR group had strong invasive ability, and the number of cells under the microscope is large. The number of cells in the siRNA group under the microscope was small, and the invasive ability is weak (P<0.05). The number of infections increased significantly, and the overall invasive ability was significantly enhanced (P<0.05). The OD values between the siRNA group and the GC group were significantly different between the two groups. The OD values of the GC group and the ANCR group were also significantly different. The proliferation of gastric cancer cells in the ANCR group was the highest, and the proliferation of the gastric cancer cells in the GC group was the least. The proliferation of gastric cancer cells in the ANCR group was significantly higher than that in the GC group. The proliferation of gastric cancer cells in the GC group was significantly higher than that in the siRNA group (P<0.05). After TUNEL staining, the apoptosis of gastric cancer cells was the highest in siRNA group, and the apoptosis of gastric cancer cells in ANCR group was less (P<0.05). The apoptosis rate of ANCR group was significantly lower than that of GC group and siRNA group (P<0.05). Western blotting was performed on GC group, siRNA group and ANCR group. The analysis showed that the siRNA group had the lowest content of PI3K and AKT protein, the ANCR group had the highest content of PI3K and AKT protein, and the ANCR group compared with GC group and siRNA group PI3K, AKT. Protein expression was significantly (all P<0.05). The results showed that the expression of PI3K and AKT mRNA was the lowest in gastric cancer cells of siRNA group, and the expression of PI3K and AKT mRNA was the highest in gastric cancer cells of ANCR group. The expression of PI3K and AKT mRNA in ANCR group was significantly higher than that in GC group and siRNA group (both P<0.05). Conclusion LncRNAANCR can activate the expression of PI3K and AKT protein, increase the invasion and proliferation of cells, promote the growth of gastric cancer cells, and accelerate the development of the disease.