Evaluation of the interaction between TGF beta and nitric oxide in the mechanisms of progression of colon carcinoma

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Serval ID
serval:BIB_344603B0BA7F
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Evaluation of the interaction between TGF beta and nitric oxide in the mechanisms of progression of colon carcinoma
Journal
Clinical and Experimental Metastasis
Author(s)
Lohm  S., Peduto-Eberl  L., Lagadec  P., Renggli-Zulliger  N., Dudler  J., Jeannin  J. F., Juillerat-Jeanneret  L.
ISSN
0262-0898 (Print)
Publication state
Published
Issued date
2005
Volume
22
Number
4
Pages
341-9
Notes
Journal Article
Research Support, Non-U.S. Gov't
Abstract
It is recognised that stromal cells determine cancer progression. We have previously shown that active TGFbeta produced by rat colon carcinoma cells modulated NO production in rat endothelial cells. To elucidate the role of TGFbeta and NO in the mechanisms of interaction of colon carcinoma cells with stromal cells and in cancer progression, we transfected REGb cells, a regressive colon carcinoma clone secreting latent TGFbeta, with a cDNA encoding for a constitutively-secreted active TGFbeta. Out of 20 injected rats only one tumour progressed, which was resected and sub-cultured (ReBeta cells). ReBeta cells secreted high levels of active TGFbeta. The adhesive properties of REGb and Rebeta cells to endothelial cells were similar, showing that the secretion of active TGFbeta is not involved in tumour cell adhesion to endothelial cells. ReBeta, but not REGb, cell culture supernatants inhibited cytokine-dependent NO secretion by endothelial cells, but inhibition of NO production was similar in co-cultures of REGb or ReBeta cells with endothelial cells. Therefore, secretion of active TGFbeta regulated endothelial NO synthase activity when tumour cells were distant from, but not in direct contact with, endothelial cells. However, only ReBeta cells inhibited cytokine-dependent secretion of NO in coculture with macrophages, indicating that the active-TGFbeta-NO axis confers an advantage for tumour cells in their interaction with macrophages rather than endothelial cells in cancer progression.
Keywords
Animals Carcinoma/*metabolism/secondary Cell Adhesion Coculture Techniques Colonic Neoplasms/*metabolism/pathology Disease Progression Endothelial Cells/metabolism Macrophages/metabolism Nitric Oxide/*metabolism Rats Rats, Inbred Strains Transforming Growth Factor beta/*metabolism Tumor Cells, Cultured
Pubmed
Web of science
Open Access
Yes
Create date
25/01/2008 8:31
Last modification date
01/10/2019 6:17
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