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Titolo:
CHOLECYSTOKININ RECEPTORS AND PANC-1 HUMAN PANCREATIC-CANCER CELLS
Autore:
SMITH JP; RICKABAUGH CA; MCLAUGHLIN PJ; ZAGON IS;
Indirizzi:
PENN STATE UNIV,MILTON S HERSHEY MED CTR,DEPT MED,DIV GASTROENTEROL,POB 850,500 UNIV DR HERSHEY PA 17033 PENN STATE UNIV,MILTON S HERSHEY MED CTR,DEPT NEUROSCI & ANAT HERSHEYPA 17033
Titolo Testata:
The American journal of physiology
fascicolo: 1, volume: 265, anno: 1993,
parte:, 1
pagine: 70000149 - 70000155
SICI:
0002-9513(1993)265:1<70000149:CRAPHP>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
ANTAGONIST RADIOLIGAND; STIMULATES GROWTH; CCK-B; RAT; BINDING; CARCINOGENESIS; SECRETIN; CERULEIN; GASTRIN; FAT;
Keywords:
L-364,718; PEPTIDE; GROWTH; L-365,260; TISSUE CULTURE; CHOLECYSTOKININ-A; CHOLECYSTOKININ-B;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
37
Recensione:
Indirizzi per estratti:
Citazione:
J.P. Smith et al., "CHOLECYSTOKININ RECEPTORS AND PANC-1 HUMAN PANCREATIC-CANCER CELLS", The American journal of physiology, 265(1), 1993, pp. 70000149-70000155

Abstract

The gastrointestinal peptide cholecystokinin (CCK) has been shown to stimulate growth of human pancreatic adenocarcinoma in vitro and in vivo, although CCK receptors have not been identified in pancreatic cancer cells. The purpose of this study was to characterize the CCK receptors in pancreatic cancer cells and to correlate the receptor binding studies with the trophic action of CCK agonists and antagonists. With the use of homogenates of PANC-1 human pancreatic cancer cell line grown in culture, the binding of I-125-labeled CCK octapeptide (I-125-CCK-8) was examined under various conditions to characterize the CCK receptor. Specific and saturable binding of I-125-CCK-8 was detected in PANC-1 cells; data were consistent with a single binding site. Scatchard analysis yielded a binding affinity [dissociation constant (K(d))] of 2.8 nM and a binding capacity of 26 fmol/mg protein. Binding was dependent on protein concentration, time, temperature, the presence of protease inhibitors, and pH and was sensitive to Na+, K+, Mg2+, and ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid. Competition experiments indicated that L-365,260, a selective CCK-B (gastrin) receptor antagonist, was the most potent displacer of I-125-CCK-8, and no significant displacement of binding was found with the selective CCK-A receptor antagonist. Growth of PANC-1 cells in culture was stimulated by CCK at a concentration consistent with the K(d), and CCK-stimulated growth was inhibited by the CCK-B receptor antagonist (L-365,260) not the CCK-A receptor antagonist (L-364,718). These results provide the first evidence that CCK-stimulated growth of human pancreatic cancer is receptor mediated and that the CCK receptors responsible forgrowth of PANC-1 human pancreatic cancer cells appear to be of the CCK-B (gastrin) type.

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Documento generato il 29/11/20 alle ore 00:10:19