Gastrin Stimulates Growth of Human Colon Cancer Cells via a Receptor Other Than CCK-A or CCK-B

Bold, Richard J.; Ishizuka, Jin; Townsend, Courtney M.; Thompson, James C.

doi:10.1006/bbrc.1994.2061

Cited by 39 publications

(27 citation statements)

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“…Recently considerable interest has developed over the possibility of other types of gastrin receptors that may mediate trophic effects [ 19,[27][28][29]. The data in these var ious studies are not consistent with a single non-A.…”

Section: Cck Receptors Activate Map Kinasecontrasting

confidence: 42%

Stimulation of both CCK-A and CCK-B Receptors Activates MAP Kinases in AR42J and Receptor-Transfected CHO Cells

et al. 1997

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It was recently found that cholecystokinin (CCK) activates mitogen-activated protein kinases (MAPK) in isolated rat pancreatic acini. The present study evaluates whether one or both types of CCK receptors are capable of MAPK activation in pancreatic AR42J acinar cells as well as CHO cells transfected with CCK-A or CCK-B receptors. CCK significantly increased p44 MAPK and p42 MAPK activities in AR42J cells. Minimal, half-maximal, and maximal responses were observed at 30 and 500 pM and 10 nM, respectively, after CCK-8 stimulation and at 100 pM and 1.5 and 30 nM, respectively, after gastrin stimulation. Glycine-extended gastrin had no effect at 100 nM and a small but significant effect at 1 μM. The CCK-B receptor antagonist L365,260 almost totally blocked MAPK activation in AR42J cells after stimulation with gastrin and glycine-extended gastrin and substantially reduced the activation of both kinases by CCK-8, while the CCK-A receptor antagonist L364J18 was much less effective. The CCK-A-selective agonist A71376, however, was an effective stimulant of MAPK activity. In an alternative approach, stably transfected CHO cells bearing either CCK-A or CCK-B receptors were stimulated with CCK-8. Each receptor induced a time-dependent increase in activity of both MAPKs by five- to sixfold in CCK-A- and CCK-B-bearing cells. In conclusion, both CCK-A and CCK-B receptors activate MAPK in AR42J cells and in transfected CHO cells.

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Section: Cck Receptors Activate Map Kinasecontrasting

confidence: 42%

Stimulation of both CCK-A and CCK-B Receptors Activates MAP Kinases in AR42J and Receptor-Transfected CHO Cells

et al. 1997

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“…Rats with cryoulcers were sacrificed 3,5,8,15,22,29,56, and 84 days after ulcer induction (three to seven rats per time point). The stomach wall containing the ulcerated tissue or the mucosal scar was frozen on dry ice and stored at -70°C, as previously described (17,31,32).…”

Section: Methodsmentioning

confidence: 99%

“…However, the molecular mechanisms that mediate these actions have not yet been identified or characterized, either in vitro or in vivo. Thus, it is not known whether the action of gastrin is a direct one at the repair site, possibly mediated through CCK receptors, the low-affinity gastrin-binding protein (21), or other distinct and not yet clearly defined receptors (22)(23)(24), or whether it acts indirectly, for instance through the stimulation of other growth factors (25).…”

mentioning

confidence: 99%

Cholecystokinin-B/gastrin receptors enhance wound healing in the rat gastric mucosa

Schmassmann¹,

Reubi²

2000

J. Clin. Invest.

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“…There is evidence for species homologues of CCK2 receptors distinguished by the relative affinities of the two stereoisomers of devazepide, R-L365260 and S-L365260, or by the differences in affinity of the agonist BC264 (Durieux et al, 1992 ]-gastrin-(1-17) and which appears to couple to the Gs family of G proteins, has been described in human colon cancer cells (Bold et al, 1994) and other cell lines (e.g. pancreatic AR42J and Swiss 3T3 fibroblasts, Seva et al, 1994;Singh et al, 1995).…”

Section: Cholecystokinin Bph_501_18 38mentioning

confidence: 99%

7tm Receptors

2009

British Journal of Pharmacology

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Overview:The completion of the Human Genome Project allowed the identification of a large family of proteins with a common motif of seven groups of 20-24 hydrophobic amino acids arranged as a helices. Approximately 800 of these seven transmembrane (7TM) receptors have been identified of which over 300 are non-olfactory receptors (see Fredriksson et al., 2003; Lagerstrom and Schioth, 2008). Subdivision on the basis of sequence homology allows the definition of rhodopsin, secretin, adhesion, glutamate and Frizzled receptor families. NC-IUPHAR recognizes Classes A, B, and C, which equate to the rhodopsin, secretin and glutamate receptor families.The nomenclature of 7TM receptors is commonly used interchangeably with G protein-coupled receptors, although the former nomenclature allows for signalling of 7TM receptors through pathways not involving G proteins. For example, adiponectin and membrane progestin receptors appear to signal independently of G proteins and appear to reside in membranes in an inverted fashion compared with conventional 7TM receptors. Additionally, the NPR3 natriuretic peptide receptor has a single transmembrane domain structure, but appears to couple to G proteins to generate cellular responses. The 300+ non-olfactory 7TM receptors are the targets for the majority of drugs in clinical usage (Overington et al., 2006), although only a minority of these receptors are exploited therapeutically. Further ReadingFoord SM, Bonner TI, Neubig RR, Rosser EM, Pin JP, Davenport AP et al. (2005) . Preliminary pairingsWhile the remainder of this section focuses on those 7TM receptors for which there is substantial pharmacological information, or interest, listed below are a number of putative 7TM receptors identified by IUPHAR , for which only preliminary evidence for an endogenous ligand has been published, or for which there exists a potential link to a disease, or disorder. Gene SymbolEnsembl ID Other names Putative endogenous ligand Comment GPR1 ENSG00000183671 -Appears to act as a co-receptor for HIV (Shimizu et al., 1999) GPR3 ENSG00000181773 ACCA Fails to respond to a variety of lipid-derived agents (Yin et al., 2009) Has been reported to activate adenylyl cyclase constitutively through Gs (Eggerickx et al., 1995). Gene disruption results in premature ovarian aging (Ledent et al., 2005) and reduced b-amyloid deposition (Thathiah et al., 2009) in mice GPR4 ENSG00000177464 Protons (Ludwig et al., 2003; Tobo et al., 2007) An initial report suggesting activation by lysophosphatidylcholine, sphingosylphosphorylcholine (Zhu et al., 2001) has been retracted (Zhu et al., 2005). Gene disruption is associated with increased perinatal mortality and impaired vascular proliferation (Yang et al., 2007 Has also been reported to respond to the phosphodiesterase inhibitor zaprinast (Taniguchi et al., 2006) and the chloride channel blocker 5-nitro-2-(3-phenylpropylamino) benzoic acid (Taniguchi et al., 2008) GPR37 ENSG00000170775 PAELR, EDNRLB Head activator peptide (Rezgaoui et al., 2006) Reported to a...

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Gastrin Stimulates Growth of Human Colon Cancer Cells via a Receptor Other Than CCK-A or CCK-B

Cited by 39 publications

References 0 publications

Stimulation of both CCK-A and CCK-B Receptors Activates MAP Kinases in AR42J and Receptor-Transfected CHO Cells

Stimulation of both CCK-A and CCK-B Receptors Activates MAP Kinases in AR42J and Receptor-Transfected CHO Cells

Cholecystokinin-B/gastrin receptors enhance wound healing in the rat gastric mucosa

7tm Receptors

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