Linked Life Data

12203118

Source:http://linkedlifedata.com/resource/pubmed/id/12203118

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
39
pubmed:dateCreated
2002-8-30
pubmed:abstractText
The arylhydrocarbon receptor (AhR) was initially identified as a member of the adaptive metabolic and toxic response pathway to polycyclic aromatic hydrocarbons and to halogenated dibenzo-p-dioxins and dibenzofurans. In the present study, we sought to determine the functional significance of the AhR pathway in pancreatic carcinogenesis. AhR expression was analysed by Northern blotting. The exact site of AhR expression was analysed by in situ hybridization and immunohistochemistry. The effects of TCDD and four selective AhR agonists on pancreatic cancer cell lines were investigated by growth assays, apoptosis assays, and induction of the cyclin-dependent kinase inhibitor p21. There was strong AhR mRNA expression in 14 out of 15 pancreatic cancer samples, weak expression in chronic pancreatitis tissues, and faint expression in all normal pancreata. In pancreatic cancer tissues, AhR mRNA and protein expression were localized in the cytoplasm of pancreatic cancer cells. TCDD and the four AhR agonists inhibited pancreatic cancer cell growth in a dose-dependent manner, and decreased anchorage-independent cell growth. DAPI staining did not reveal nuclear fragmentation and CYP1A1 and was not induced by TCDD and AhR agonists. In contrast, TCDD and AhR agonists induced the expression of the cyclin-dependent kinase inhibitor p21. In conclusion, the relatively non-toxic AhR agonists caused growth inhibition in pancreatic cancer cells with high AhR expression levels via cell cycle arrest. In addition, almost all human pancreatic cancer tissues expressed this receptor at high levels, suggesting that these or related compounds may play a role in the therapy of pancreatic cancer in the future.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6059-70
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed-meshheading:12203118-Adenocarcinoma, pubmed-meshheading:12203118-Adult, pubmed-meshheading:12203118-Aged, pubmed-meshheading:12203118-Blotting, Northern, pubmed-meshheading:12203118-Cell Adhesion, pubmed-meshheading:12203118-Chronic Disease, pubmed-meshheading:12203118-Cyclin-Dependent Kinase Inhibitor p21, pubmed-meshheading:12203118-Cyclins, pubmed-meshheading:12203118-Cytochrome P-450 CYP1A1, pubmed-meshheading:12203118-Environmental Pollutants, pubmed-meshheading:12203118-Female, pubmed-meshheading:12203118-Humans, pubmed-meshheading:12203118-Immunoenzyme Techniques, pubmed-meshheading:12203118-In Situ Hybridization, pubmed-meshheading:12203118-Male, pubmed-meshheading:12203118-Middle Aged, pubmed-meshheading:12203118-Pancreatic Neoplasms, pubmed-meshheading:12203118-Pancreatitis, pubmed-meshheading:12203118-RNA, Messenger, pubmed-meshheading:12203118-Receptors, Aryl Hydrocarbon, pubmed-meshheading:12203118-Tetrachlorodibenzodioxin, pubmed-meshheading:12203118-Tumor Cells, Cultured
pubmed:year
2002
pubmed:articleTitle
Increased arylhydrocarbon receptor expression offers a potential therapeutic target for pancreatic cancer.
pubmed:affiliation
Department of Visceral and Transplantation Surgery, University of Bern, Inselspital, Switzerland.
pubmed:publicationType
Journal Article