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. 2013 Oct 31;306(2):G91–G101. doi: 10.1152/ajpgi.00301.2013

Fig. 2.

Fig. 2.

The proliferative actions of CCK and gastrin on PANC-1 pancreatic cancer cell are mediated through the CCK-B receptor, not the CCK-A receptor. A: growth of PANC-1 cells, which have both CCK-A and CCK-B receptors, was tested in the presence of saline (control), CCK (10−9 M) alone, or CCK (10−9 M) in the presence of the CCK-A receptor antagonist L-364,718 (10−9 M) or the CCK-B/gastrin receptor antagonist L-365,260 (10−9 M), and each antagonist alone. CCK stimulated cell growth that was only blocked by the CCK-B receptor antagonist, not the CCK-A antagonist. From Ref. 81. B: gastrin exerts a similar but even greater proliferative effect on growth of PANC-1 cells via the CCK-B receptor. Gastrin (10−9 M) significantly increases cell number compared with control cells. The proliferative effects of gastrin are not altered in the presence of the CCK-A receptor antagonist L-364,718 (10−9 M) but are blocked by the CCK-B/gastrin receptor antagonist L-365,260 (10−9 M), at concentrations of antagonist that do not effect growth alone. Studies were performed in PANC-1 cells in serum-free medium over 6 days (P < 0.005). From Ref. 75.