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From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Sun, Mar 16, 2008 at 1:55 AM
Subject: Role for epithelial dysregulation in early-onset colitis-associated colon cancer in Gi2-alpha-/- mice.
To: mesothelioma77@gmail.com
[1]Inflamm Bowel Dis. 2008 Mar 13;
Edwards RA, Wang K, Davis JS, Birnbaumer L
Background: Inflammatory bowel disease (IBD) is a risk factor for developing colorectal cancer but the mechanisms are poorly characterized. Mice lacking the G-protein alpha subunit Gi2-alpha spontaneously develop colitis and colon cancer with high penetrance. Compared to canonical Wnt/APC signaling-based animal models of colon cancer, the tumors in Gi2-alpha-/- mice more closely recapitulate the features of IBD-associated cancers seen in humans. They are predominantly right-sided, multifocal, mucinous, and arise from areas of flat dysplasia.Methods: In evaluating the potential contribution of epithelial Gi2-alpha signaling to this phenotype, we found that Gi2-alpha-/- colonic epithelium is hyperproliferative even before the onset of colitis, and resistant to the induction of apoptosis. We generated colon cancer cell lines overexpressing dominant-negative Gi2-alpha.Results: Like other cells lacking Gi2-alpha, these cells release less arachidonic acid, an important antiinflammatory and epithelial growth regulator. They are also hyperproliferative and resistant to camptothecin-induced apoptosis and caspase-3 activation.Conclusions: The colitis-associated cancers in Gi2-alpha-/- mice appear very similar to those seen in human IBD patients, and Gi2-alpha is a direct negative regulator of colonic epithelial cell growth.(Inflamm Bowel Dis 2008).
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Source: http://www.hubmed.org/display.cgi?uids=18340649
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From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Sun, Mar 16, 2008 at 1:55 AM
Subject: Role for epithelial dysregulation in early-onset colitis-associated colon cancer in Gi2-alpha-/- mice.
To: mesothelioma77@gmail.com
[1]Inflamm Bowel Dis. 2008 Mar 13;
Edwards RA, Wang K, Davis JS, Birnbaumer L
Background: Inflammatory bowel disease (IBD) is a risk factor for developing colorectal cancer but the mechanisms are poorly characterized. Mice lacking the G-protein alpha subunit Gi2-alpha spontaneously develop colitis and colon cancer with high penetrance. Compared to canonical Wnt/APC signaling-based animal models of colon cancer, the tumors in Gi2-alpha-/- mice more closely recapitulate the features of IBD-associated cancers seen in humans. They are predominantly right-sided, multifocal, mucinous, and arise from areas of flat dysplasia.Methods: In evaluating the potential contribution of epithelial Gi2-alpha signaling to this phenotype, we found that Gi2-alpha-/- colonic epithelium is hyperproliferative even before the onset of colitis, and resistant to the induction of apoptosis. We generated colon cancer cell lines overexpressing dominant-negative Gi2-alpha.Results: Like other cells lacking Gi2-alpha, these cells release less arachidonic acid, an important antiinflammatory and epithelial growth regulator. They are also hyperproliferative and resistant to camptothecin-induced apoptosis and caspase-3 activation.Conclusions: The colitis-associated cancers in Gi2-alpha-/- mice appear very similar to those seen in human IBD patients, and Gi2-alpha is a direct negative regulator of colonic epithelial cell growth.(Inflamm Bowel Dis 2008).
___
Source: http://www.hubmed.org/display.cgi?uids=18340649
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