« Previous
Next »
Cancer Letters
Volume 222, Issue 1
, Pages 95-105
, 10 May 2005
Analysis of the cellular and molecular mechanisms of trophic action of a misspliced form of the type B cholecystokinin receptor present in colon and pancreatic cancer
References
- G protein-coupled cholecystokinin-B/gastrin receptors are responsible for physiological cell growth of the stomach mucosa in vivo. Proc. Natl Acad. Sci. USA. 1996;93:11825–11830
- . The role of gastrin and cholecystokinin in normal and neoplastic gastrointestinal growth. J. Gastroenterol. Hepatol. 1995;10:215–232
- . CCK stimulates growth of six human pancreatic cancer cell lines in serum-free medium. Regul. Pept. 1991;32:341–349
- . Molecular mechanisms for the growth factor action of gastrin. Am. J. Physiol. Gastrointest. Liver Physiol. 1997;273:G891–G898
- . Stimulation of both CCK-A and CCK-B receptors activates MAP kinases in AR42J and receptor-transfected CHO cells. Digestion. 1997;58:361–367
- . Cell type-specific requirement of the MAPK pathway for the growth factor action of gastrin. Am. J. Physiol. Gastrointest. Liver Physiol. 1999;276:G1363–G1372
- . Gastrin-induced DNA synthesis requires p38-MAPK activation via PKC/Ca2+ and Src-dependent mechanisms. FEBS Lett. 2001;496:25–30
- . CCK-B receptors produce similar signals but have opposite growth effects in CHO and Swiss 3T3 cells. Am. J. Physiol. Cell Physiol. 1997;273:C1449–C1457
- . Clinical significance of gastrin receptors in human colon cancers. Cancer Res. 1989;49:488–492
- . Cholecystokinin receptors and PANC-1 human pancreatic cancer cells. Am. J. Physiol. Gastrointest. Liver Physiol. 1993;265:G149–G155
- . Characterization of the CCK-B/gastrin-like receptor in human colon cancer. Am. J. Physiol. Regul. Integr. Comp. Physiol. 1996;271:R797–R805
- . Cholecystokinin A and B receptors are differentially expressed in normal pancreas and pancreatic adenocarcinoma. J. Clin. Invest. 1997;100:597–603
- . Human colorectal cancers express a constitutively active cholecystokinin-B/gastrin receptor that stimulates cell growth. J. Biol. Chem. 2000;275:32122–32128
- . A misspliced form of the cholecystokinin-B/gastrin receptor in pancreatic carcinoma: role of reduced cellular U2AF35 and a suboptimal 3′-splicing site leading to retention of the fourth intron. Cancer Res. 2002;62:947–952
- . Characterization of the CCK-C (cancer) receptor in human pancreatic cancer. Int. J. Mol. Med. 2002;10:689–694
- . Molecular characterization and organ distribution of type A and B cholecystokinin receptors in cynomolgus monkey. Am. J. Physiol. Gastrointest. Liver Physiol. 2001;281:G507–G514
- . Relationship between native and recombinant cholecystokinin receptors-role of differential glycosylation. Pancreas. 1996;13:130–139
- . LIGAND: a versatile computerized approach for characterization of ligand-binding systems. Anal. Biochem. 1980;107:220–239
- . Novel tool for the study of cholecystokinin-stimulated pancreatic enzyme secretion. J. Clin. Invest. 1989;83:321–325
- . Heterodimerization of type A and B cholecystokinin receptors enhance signaling and promote cell growth. J. Biol. Chem. 2003;278:52972–52979
- . Environment and mobility of a series of fluorescent reporters at the amino terminus of structurally related peptide agonists and antagonists bound to the cholecystokinin receptor. J. Biol. Chem. 2002;277:18552–18560
- . The human gastrin/cholecystokinin type B receptor gene: alternative splice donor site in exon 4 generates two variant mRNAs. Proc. Natl Acad. Sci. USA. 1993;90:9085–9089
- Dual pathways of internalization of the cholecystokinin receptor. J. Cell Biol. 1995;128:1029–1042
- . Gastrin, CCK, signaling, and cancer. Annu. Rev. Physiol. 2001;63:49–76
- . Calcium—a life and death signal. Nature. 1998;395:645–648
- . Calcium oscillations in single cultured Chinese hamster ovary cells stably transfected with a cloned human cholecystokinin (CCK)B receptor. Jpn. J. Pharmacol. 1997;75:33–42
- . Correlation between Ca(2+) oscillation and cell proliferation via CCK(B)/gastrin receptor. Biochim. Biophys. Acta. 1999;1452:243–253
☆ This work was supported by grants from the National Institutes of Health, DK32878, the Fiterman Foundation, and by the Kendall-Mayo Fellowship Award (Z.-J.C.).
PII: S0304-3835(04)00713-X
doi: 10.1016/j.canlet.2004.09.008
© 2004 Elsevier Ireland Ltd. All rights reserved.
« Previous
Next »
Cancer Letters
Volume 222, Issue 1
, Pages 95-105
, 10 May 2005
