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Titolo:
MODULATION OF APOPTOSIS AND BCL-2 EXPRESSION BY PROSTAGLANDIN E-2 IN HUMAN COLON-CANCER CELLS
Autore:
SHENG HM; SHAO JY; MORROW JD; BEAUCHAMP RD; DUBOIS RN;
Indirizzi:
VANDERBILT UNIV,MED CTR,DEPT MED GI,MCN C-2104 NASHVILLE TN 37232 VANDERBILT UNIV,MED CTR,DEPT MED NASHVILLE TN 37232 VANDERBILT UNIV,MED CTR,DEPT CELL BIOL NASHVILLE TN 37232 VANDERBILT UNIV,MED CTR,DEPT SURG NASHVILLE TN 37232 VANDERBILT UNIV,MED CTR,CTR MOL TOXICOL NASHVILLE TN 37232 VET AFFAIRS MED CTR NASHVILLE TN 37232
Titolo Testata:
Cancer research
fascicolo: 2, volume: 58, anno: 1998,
pagine: 362 - 366
SICI:
0008-5472(1998)58:2<362:MOAABE>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTESTINAL EPITHELIAL-CELLS; CYCLOOXYGENASE-2 LEVELS; PHORBOL ESTER; IN-VIVO; GENE; SYNTHASE-2; CARCINOMA; POLYPOSIS; INHIBITOR; ADENOMAS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
33
Recensione:
Indirizzi per estratti:
Citazione:
H.M. Sheng et al., "MODULATION OF APOPTOSIS AND BCL-2 EXPRESSION BY PROSTAGLANDIN E-2 IN HUMAN COLON-CANCER CELLS", Cancer research, 58(2), 1998, pp. 362-366

Abstract

Previously, we have shown that forced expression of prostaglandin endoperoxide synthase-2 [also called cyclooxygenase (COX) 2] leads to inhibition of programmed cell death in intestinal epithelial cells, More recently, we have demonstrated that growth of human colonic cancer xenografts is inhibited by treatment with a highly selective COX-2 inhibitor in tumors that express COX-2 (HCA-7) but not in those that lack COX-2 expression (HCT-116). To explore the biochemical mechanisms involved in these effects, we have evaluated the role of COX-2-derived eicosanoid products on programmed cell death in human colon cancer cells, Here we report that PGE(2) treatment of human colon cancer cells leads to increased clonogenicity of HCA-7, but not HCT-116 cells, Treatment with a highly selective COX-2 inhibitor (SC-58125) decreases colony formation in monolayer culture and this growth inhibition was reversed by treatment with PGE(2). Additionally, PGE(2) inhibits programmed celldeath caused by SC-58125 and induces Bcl-2 expression, but did not affect Bcl-x or Bax expression in human colon cancer (HCA-7) cells, Therefore, decreased cell death caused by PGE(2) would enhance the tumorigenic potential of intestinal epithelial cells, Thus, these results mayhelp to explain a component of the mechanism by which COX inhibitors prevent colorectal cancer in humans.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 09:31:26