62. Effect of P13K signal pathway to distribution and expression of Phosphorylated P27 in gastric cancer cell

Objective: To investigate the expression and distribution of protein P27 and Phosphorylated P27 (p-P27) in gastric cancer cell lines (BGC-823), when the PI3K pathway was inhibited. Methods: The cell line BGC-823 was cultivated, and treated by LY294002, the PI3K pathway inhibitor. Cell cycle was determined by Flow cytometry. The expression of protein P27, p-P27 (Thr187), p-P27 (Thr157) and p-P27 (Ser10) in total cell, cytoplasm and nuclear were analyzed by Western blotting respectively.
Results: Inhibiting PI3K pathway caused cell arrest and increased in G1 population [treat cell vs. Control cells was (83.9% vs. 67.6%, P=0.001)]. To compare with the treated group and the control group, the expression of protein P27 was significantly increase in total cell, cytoplasm and nuclei, respectively (P=0.000, 0.000, 0.001). The expression of p-P27 (Ser10) was significantly decrease in total cell, cytoplasm and nuclei, respectively (P=0.000, 0.001, 0.001). The expression of p-P27 (Thr157) was significantly decrease in total cell and cytoplasm, respectively (P=0.001, 0.001). The expression of p-P27 (Thr157) in nuclei was decrease, but it was no statistically difference (P=0.482). The expression of p-P27 (Thr187) was decrease in total cell and cytoplasm, and increase in nuclei, but they were no statistically difference, respectively (P=0.254, 0.070, 0.223).
Conclusions: When PI3K pathway was inhibited in gastric cancer cell, the expression of protein P27 was up-regulated and the expression of p-P27 was down-regulated. Moreover, the distribution of P27 and p-P27 in the cytoplasm and nuclei were altered. Inhibiting PI3K pathway induced gastric cancer cells arrest in G1, and caused cell apoptosis.