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¹ Department of Biology, University ‘Roma Tre’, Viale G Marconi 446, I-00146 Rome, Italy
² Interdepartmental Laboratory for Electron Microscopy, University ‘Roma Tre’, Via della Vasca Navale 79, I-00146 Rome, Italy

(Requests for offprints should be addressed to M Marino; Email: m.marino{at}uniroma3.it)

F Acconcia is now at Department of Molecular and Cellular Oncology, MD Anderson Cancer Center, 1515 Holcombe Boulevard, Texas Medical Center, Houston, Texas 77030, USA

Nitric oxide (NO) and 17ß-estradiol (E2) are both important in gastrointestinal health and disease. NO contributes to gastrointestinal motility as well as to inflammation and carcinogenic processes. By contrast, E2 reduces the incidence of colon adenoma and carcinoma by about 30%. We report the genomic and non-genomic E2–estrogen receptor (ER) ß-induced effects in human colon adenocarcinoma. The effect of NO on ERß activities was also assessed. The E2-ERß-dependent gene transcription was inhibited by exogenous NO, whereas some non-genomic E2-dependent effects (e.g. p38/MAP kinase), important for the activation of the apoptotic cascade, were unaffected by NO. However, NO impaired the E2-induced pro-apoptotic cascade in human colon adenocarcinoma cells by inhibiting caspase-3. The effects of NO may reflect chemical modification(s) of Cys residues present in the DNA recognition domain of ERß as well as in the caspase-3 active site. On the whole, high NO concentrations suppressed the E2 protective effects in the gastrointestinal tract, suggesting that the caspase-dependent apoptotic cascade may become critical under conditions of high redox stress such as occur under specific activation of the immune system by chronic infections or pathogen challenge.

This article has been cited by other articles:

				P. Galluzzo, F. Caiazza, S. Moreno, and M. Marino Role of ER{beta} palmitoylation in the inhibition of human colon cancer cell proliferation Endocr. Relat. Cancer, March 1, 2007; 14(1): 153 - 167. [Abstract] [Full Text] [PDF]