Author/Authors :
Xu، نويسنده , , Wei and Chen، نويسنده , , Guo-Sheng and Shao، نويسنده , , Yun and Li، نويسنده , , Xiao-Lin and Xu، نويسنده , , Haichen and Zhang، نويسنده , , Hao and Zhu، نويسنده , , Guo-Qing and Zhou، نويسنده , , Yi-Chan and He، نويسنده , , Xiao-Pu and Sun، نويسنده , , Wei-Hao، نويسنده ,
Abstract :
Gastrin, cholecystokinin2 receptor (CCK2R), and cyclooxygenase-2 (COX-2) have been implicated in the carcinogenesis and progression of gastric cancer. Our study demonstrated that antagonist or siRNA against CCK2R blocked amidated gastrin (G17)-induced activation of STAT3 and Akt in gastric cancer cell lines. G17-increased COX-2 expression and cell proliferation were effectively blocked by CCK2R antagonist and inhibitors of JAK2 and PI3K. In addition, knockdown of STAT3 expression significantly attenuated G17-induced PI3K/Akt activation, COX-2 expression, and cell proliferation. These results suggest that CCK2R-mediated COX-2 up-regulation via JAK2/STAT3/PI3K/Akt pathway is involved in the proliferative effect of G17 on human gastric cancer cells.
Keywords :
PI3K/AKT , Gastric cancer , Cholecystokinin2 receptor , Cyclooxygenase-2 , JAK2/STAT3
