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A pharmacological analysis of the cholinergic regulation of urokinase-type plasminogen activator secretion in the human colon cancer cell line, HT-29
Karlstad University, Faculty of Technology and Science, Department of Chemistry and Biomedical Sciences.
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2010 (English)In: European Journal of Pharmacology, ISSN 0014-2999, Vol. 646, no 1,2,3, p. 22-30Article in journal (Refereed) Published
Abstract [en]

Urokinase-type plasminogen activator (uPA) is an important factor for tumour cell invasion and metastasis. We recently showed that acetylcholine is an autocrine/paracrine growth factor for the human colon cancer cell line, HT-29, in part via the 7 subtype of the nicotinic acetylcholine receptors. In the current study, we investigated whether acetylcholine participates in the regulation of the protein expressions of also uPA and its receptor (uPAR) in the HT-29 cell line. Such were investigated by immunocytochemistry and Western blotting, and quantitation of uPA secretion was undertaken by ELISA. Stimulation of the cells for 24h with nicotine caused increased uPA secretion with peak effect (78% above the control) occurring at a nicotine concentration of 10nM. This effect was markedly inhibited by -Bungarotoxin, thus showing the involvement of 7 nicotinic acetylcholine receptors. Basal uPA secretion was found to be partly dependent on ongoing activation of nicotinic receptors, suggesting tonic production of acetylcholine. Conversely, there was no cholinergic influence on the expression of uPAR. The current findings demonstrate novel aspects of receptor-mediated regulation of tumour metastatic potential via uPA secretion. This may suggest future pharmaceutical strategies in treatment of colorectal cancer.

Place, publisher, year, edition, pages
Elsevier, 2010. Vol. 646, no 1,2,3, p. 22-30
National Category
Biological Sciences
Research subject
Biomedical Science
Identifiers
URN: urn:nbn:se:kau:diva-10572DOI: 10.1016/j.ejphar.2010.08.004OAI: oai:DiVA.org:kau-10572DiVA, id: diva2:494115
Available from: 2012-02-08 Created: 2012-02-08 Last updated: 2015-06-25Bibliographically approved

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Publisher's full texthttp://www.ncbi.nlm.nih.gov/pubmed/20727878

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