Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Dysregulation of integrin-linked kinase (ILK) signaling in colonic polyposis
Autore:
Marotta, A; Tan, C; Gray, V; Malik, S; Gallinger, S; Sanghera, J; Dupuis, B; Owen, D; Dedhar, S; Salh, B;
Indirizzi:
Jack Bell Res Ctr, Vancouver, BC V6H 3Z6, Canada Jack Bell Res Ctr Vancouver BC Canada V6H 3Z6 ncouver, BC V6H 3Z6, Canada British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada British ColumbiaCanc Agcy Vancouver BC Canada V5Z 4E6 BC V5Z 4E6, Canada Thunderbay Reg Hosp, Thunder Bay, ON P7E 1G6, Canada Thunderbay Reg Hosp Thunder Bay ON Canada P7E 1G6 Bay, ON P7E 1G6, Canada Mt Sinai Hosp, Toronto, ON M5G 1X5, Canada Mt Sinai Hosp Toronto ON Canada M5G 1X5 Hosp, Toronto, ON M5G 1X5, Canada Kinetek Pharmaceut Inc, Vancouver, BC V6P 6PA, Canada Kinetek Pharmaceut Inc Vancouver BC Canada V6P 6PA er, BC V6P 6PA, Canada Vancouver Gen Hosp, Vancouver, BC V5Z 1M9, Canada Vancouver Gen Hosp Vancouver BC Canada V5Z 1M9 couver, BC V5Z 1M9, Canada
Titolo Testata:
ONCOGENE
fascicolo: 43, volume: 20, anno: 2001,
pagine: 6250 - 6257
SICI:
0950-9232(20010927)20:43<6250:DOIK(S>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
NONSTEROIDAL ANTIINFLAMMATORY DRUGS; PROSTATE-CANCER CELLS; CYCLIN D1 GENE; BETA-CATENIN; PROTEIN-KINASE; CYCLOOXYGENASE-2 INHIBITOR; ANTICANCER AGENTS; SULINDAC SULFIDE; UP-REGULATION; APC;
Keywords:
intestinal polyposis; integrin-linked kinase (ILK); non-steroidal anti-inflammatory drugs (NSAIDs); adenomatous polyposis coli (APC); beta-catenin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Salh, B Jack Bell Res Ctr, 2660 Oak St, Vancouver, BC V6H 3Z6, Canada JackBell Res Ctr 2660 Oak St Vancouver BC Canada V6H 3Z6 , Canada
Citazione:
A. Marotta et al., "Dysregulation of integrin-linked kinase (ILK) signaling in colonic polyposis", ONCOGENE, 20(43), 2001, pp. 6250-6257

Abstract

Mutation of the adenomatous polyposis coli (APC) gene and the subsequent dysregulation of beta -catenin are well-documented abnormalities in familialadenomatous polyposis (FAP), as well as sporadic polyposis. Intriguingly, overexpression of the integrin-linked kinase (ILK) has been shown to modulate beta -catenin subcellular localization and function. However, the significance of this finding for human carcinogenesis remains unclear. Here, we report the increased biochemical activity and expression of ILK protein in polyps from FAP patients. Furthermore, dramatic increases in ILK immunoreactivity were observed in all abnormal crypts from sporadic polyps, when compared with the normal appearing crypts within the same resected specimens. Assulindac and aspirin are the two most important therapeutic/chemopreventative agents demonstrated in colorectal carcinogenesis, in both humans and animals, further investigation revealed that these non-steroidal antiinflammatory drugs (NSAIDs) target ILK and ILK-mediated events in vivo. These include inhibition of, both the biochemical activation of ILK, inhibition of serine 9 GSK3 beta phosphorylation and the enhancement of TCF-4 transcriptional activity. In conclusion, ILK protein hyperexpression appears to be an early event in colonic polyposis. Additionally, ILK signaling is shown to undergo modulation by sulindac (and aspirin) for the first time, indicating that it is likely to be one of the targets affected by these agents in vivo.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 10:21:49