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.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Xu W,Chen GS,Shao Y,Li XL,Xu HC,Zhang H,Zhu GQ,Zhou YC,He XP,Sun WHdoi
10.1016/j.canlet.2012.12.030subject
Has Abstractpub_date
2013-05-10 00:00:00pages
11-8issue
1eissn
0304-3835issn
1872-7980pii
S0304-3835(13)00083-9journal_volume
332pub_type
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