Add like
Add dislike
Add to saved papers

Augmented O -GlcNAcylation alleviates inflammation-mediated colon carcinogenesis via suppression of acute inflammation.

Colon cancer prevalence is high worldwide. O -GlcNAcylation has been associated with tumor growth in various tissues, including the colon; however, its link to carcinogenesis is not fully understood. We investigated the association of O -GlcNAcylation with colon carcinogenesis using a 1,2-dimethylhydrazine/dextran sodium sulfate-induced colon carcinogenesis model in wild type and O -GlcNAc transferase-transgenic ( Ogt -Tg) mice. The incidence of colon cancer was significantly lower in Ogt -Tg than in wild type mice. The colonic length was not shortened in Ogt -Tg mice, and NF-κB p65 phosphorylation was strongly suppressed, indicating that reduction of inflammation might be related to the alleviation of colon carcinogenesis. Dextran sodium sulfate-induced acute colitis mice were used to evaluate the effect of O -GlcNAcylation on inflammation at the maximal inflammation period. In Ogt -Tg mice, NF-κB p65 phosphorylation and interleukin-1β mRNA expression were suppressed. Histochemical staining demonstrated shedding of colon epithelial cells in wild type mice a few days after dextran sodium sulfate treatment, whereas they remained essentially intact in Ogt -Tg mice. There were no significant differences on histochemical staining in the remaining epithelia between groups. These data suggest that O -GlcNAcylation could prevent colon carcinogenesis through reducing acute maximum inflammation, suggesting modulation of O -GlcNAcylation as a novel therapeutic option.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app