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Effects of Gastrin on 3',5'-Cyclic Adenosine Monophosphate, Intracellular Calcium, and Phosphatidylinositol Hydrolysis in Human Colon Cancer Cells¹

Department of Surgery, The University of Texas Medical Branch, Galveston, Texas 77555 [J. I., C. M. T., Jr., R. J. B., J. C. T.] and Centre CNRS-INSERM de Pharmacologie-Endocrinologie, Rue de la Cardonille, 34094 Montepellier, Cedex 5, France [J. M., M. R.]

Gastrin is a trophic factor for some human colon cancer cells. However, the signal-transduction pathways by which gastrin regulates growth are still unknown. We examined the effect of synthetic human gastrin-17 (G-17) on signal-transduction pathways and cell growth using 4 different human colon cancer cell lines (LoVo, COLO 320, HT-29, and HCT116). G-17 stimulated the production of cyclic AMP in LoVo, COLO 320, and HCT116 cells, while G-17 stimulated phosphatidylinositol hydrolysis and mobilization of intracellular calcium in HT-29 cells. The growth-regulatory effect of G-17 on these colon cancer cells (stimulatory on LoVo, COLO 320, and HT-29 cells; inhibitory on HCT116 cells) was well correlated with the effect of G-17 on the signal-transduction pathway in each cell line. We further examined the effect of a selective cholecystokinin-B type receptor antagonist, JMV 320, on G-17-induced signal-transduction pathways and G-17-regulated growth. In each cell line, the effect of JMV 320 on G-17-induced signal-transduction pathways was well correlated with that on G-17-regulated growth. G-17 appears to regulate, at least to some extent, growth of human colon cancer cells through gastrin receptor-linked signal-transduction pathways that are cell-specific.

¹ Supported by grants from the NIH (5R37 DK 15241 and P01 DK 35608), American Cancer Society (CB-571), Walls Medical Research Foundation, and the John Sealy Memorial Endowment Fund.

² To whom requests for reprints should be addressed, at Department of Surgery, Route E-33, 6.136 Old John Sealy, The University of Texas Medical Branch, Galveston, TX 77555-0533.

Received 8/27/93. Accepted 2/18/94.

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