Do neuro-humoral signaling molecules participate in colorectal carcinogenesis/cancer progression?
2012 (English)In: Neurogastroenterology and Motility, ISSN 1350-1925, E-ISSN 1365-2982, Vol. 24, no 2, p. 96-99Article in journal (Refereed) Published
Resource type
Text
Abstract [en]
Signaling molecules in the gastrointestinal (GI) tract, as released from intrinsic, or extrinsic neurons, or from local endocrine cells may serve as positive or negative growth factors, and it has been suggested that such could participate also in colorectal carcinogenesis/cancer progression. Sporadic colorectal cancer arises from an initially benign adenoma, which, in turn, develops from the stem cell compartment, located in the bottom of the crypts of the colorectal mucosa. It was recently demonstrated in rat that intrinsic denervation of the colon appeared to be protective against chemically induced carcinogenesis. Of the various GI signaling molecules, noradrenaline (NA) and substance P (SP) may be of particular importance as growth factors involved in colorectal cancer. In the current issue of Neurogastroenterology and Motility, Graf et al. demonstrate that in benign, human colon polyps, there was a loss of innervation compared with adjacent mucosa, affecting efferent, noradrenergic, as well as sensory, SP-ergic fibers, while there was an increase in SP-immunoreactive non-neuronal cells in the polyps. The results obtained could suggest that loss of mucosal innervation, due to e.g. luminal, pro-inflammatory stimuli, could result in unbalanced pro-tumorigenic stimulation of the stem cell region by non-neuronal SP. The current findings may be important for the further understanding of the development of sporadic colorectal cancer.
Place, publisher, year, edition, pages
Wiley-Blackwell, 2012. Vol. 24, no 2, p. 96-99
Keywords [en]
colorectal cancer, enteric nerves, extrinsic nerves, noradrenaline, substance P
National Category
Biomedical Laboratory Science/Technology
Research subject
Biomedical Sciences
Identifiers
URN: urn:nbn:se:kau:diva-41850DOI: 10.1111/j.1365-2982.2011.01854.xISI: 000299099800003OAI: oai:DiVA.org:kau-41850DiVA, id: diva2:923067
2016-04-252016-04-222020-05-19Bibliographically approved