ArticleIn vitro cellular & developmental biology. Animal2009
Transforming growth factor-beta1 (TGF-beta1) and acetylcholine (ACh) alter nitric oxide (NO) and interleukin-1beta (IL-1beta) secretion in human colon adenocarcinoma cells.
Article in In vitro cellular & developmental biology. Animal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Review
- Opioids, Neutral Endopeptidase, its Inhibitors and Cancer: Is There a Relationship among them?Archivum immunologiae et therapiae experimentalis · 2015Review
- Extrinsic intestinal denervation modulates tumor development in the small intestine of Apc(Min/+) mice.Journal of experimental & clinical cancer research : CR · 2015Article
- Mutual modulation between norepinephrine and nitric oxide in haemocytes during the mollusc immune response.Scientific reports · 2014Article
- ZNF580 mediates eNOS expression and endothelial cell migration/proliferation via the TGF-β1/ALK5/Smad2 pathway.Molecular and cellular biochemistry · 2014Article
- The effect of transforming growth factor-beta1 on nasopharyngeal carcinoma cells: insensitive to cell growth but functional to TGF-beta/Smad pathway.Journal of experimental & clinical cancer research : CR · 2010Article
- The tumor microenvironment in colorectal carcinogenesis.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2010Article
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2 authors at 1 institution in 1 country.
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Abstract
Colon adenocarcinoma is one of the most common fatal malignancies in Western countries. Progression of this cancer is dependent on tumor microenvironmental signaling molecules such as transforming growth factor-beta (TGF-beta) or acetylcholine (ACh). The present study was conducted to assess the influence of recombinant human transforming growth factor (rhTGF)-beta1 or ACh on nitric oxide (NO) and interleukin-1beta (IL-1beta) secretion by three human colon adenocarcinoma cell lines: HT29, LS180, and SW948, derived from different grade tumors (Duke's stage). The cells were cultured in 2D and 3D (spheroids) conditions. Colon carcinoma cells exhibited different sensitivities to rhTGF-beta1 or ACh dependent on the tumor grade and the culture model. ACh exhibited significant inhibitory effects towards NO, endothelial nitric oxide synthase (eNOS), and IL-1beta secretion especially by tumor cells derived form Duke's C stage of colon carcinoma. rhTGF-beta1 also decreased NO, IL-1beta, and eNOS expression, but its effect was lower than that observed after the administration of ACh. The inhibition of NO and IL-1beta production was more striking in 3D tumor spheroids than in 2D culture monolayers. Taken together, the TGF-beta1-ACh axis may regulate colon carcinoma progression and metastasis by altering NO secretion and influence inflammatory responses by modulating IL-1beta production.
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