Is acetylcholine a signaling molecule for human colon cancer progression?
2011 (English)In: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, E-ISSN 1502-7708, Vol. 46, no 4, 446-455 p.Article in journal (Refereed) PublishedText
Objective. Non-neuronal acetylcholine (ACh) has been suggested to be a mediator for the development of various types of cancer. We analyzed a possible role for this molecule in carcinogenesis and/or progression of human colon cancer, in patient biopsies harvested from the colon during surgery. We addressed whether ACh synthesis (by choline acetyltransferase) and/or degradation (by ACh esterase), as well as the expression of the alpha alpha 7-subtype of the nicotinic ACh receptors, and the peptide ligand at the alpha alpha 7 receptors, secreted mammalian Ly6/urokinase-type plasminogen activator receptor-related protein-1, respectively, are deranged in tumor tissue as compared with macroscopically tumor-free colon tissue. Methods. A total of 38 patients were grouped for analysis based on their respective Dukes stage (either Dukes A ++ B or C ++ D). A mucosal tissue sample was harvested from macroscopically tumor-free colon tissue (i.e. control tissue), as well as from the tumor, and protein lysates were prepared for quantitative Western blotting. Full-thickness specimens were taken for immunohistochemistry. Results. For all the above named markers, there was a significant difference between control and tumor tissue with regard to protein levels, and there was, in addition, a significant difference in protein levels between the Dukes A ++ B and C ++ D groups. Conclusion. The current findings may suggest a role for ACh in colon carcinogenesis/cancer progression; the data obtained could have prognostic and/or therapeutic significance for this disease.
Place, publisher, year, edition, pages
2011. Vol. 46, no 4, 446-455 p.
Acetylcholine, choline acetyltransferase, colon cancer, nicotinic acetylcholine receptor, SLURP-1
Research subject Biomedical Sciences
IdentifiersURN: urn:nbn:se:kau:diva-40631DOI: 10.3109/00365521.2010.539252ISI: 000288170600009PubMedID: 21265716OAI: oai:DiVA.org:kau-40631DiVA: diva2:905463