Abstract
Obesity is rapidly becoming a global phenomenon. This is more than a cosmetic issue as obesity is associated with several life-threatening diseases, including colon cancer. Insulin resistance and inflammation, underlying factors in obesity-related diseases, promote colonocyte proliferation and suppress programmed cell death, or apoptosis, by activating the insulin-like growth factor (IGF) and prostaglandin pathways. These pathways converge on the Wnt pathway, which is implicated in colon carcinogenesis. Despite tremendous advances in our understanding of the molecular mechanisms involved in colon carcinogenesis, mortality due to colon cancer world-wide is unacceptably high. Even though conventional therapies can prolong a patients life-span a few years, they cause serious side effects. Thus, there is growing interest in functional foods and dietary bioactive compounds with chemopreventive properties. This search is fueled by the epidemiological studies indicating that plant-based diets are protective against several types of cancers. This review provides a brief summary of the IGF and prostaglandin pathways, which are implicated in obesity-enhanced colon cancer, and some of the functional foods/dietary compounds that target these pathways. It is essential to understand the molecular mechanisms involved in chemoprevention before providing appropriate science-based dietary recommendations to prevent colon cancer in both obese and non-obese individuals.
Keywords: Colon cancer, functional foods, obesity, Wnt, prostaglandin, IGF, insulin, inflammation
Current Cancer Drug Targets
Title: Obesity-Enhanced Colon Cancer: Functional Food Compounds and their Mechanisms of Action
Volume: 8 Issue: 7
Author(s): Jairam Vanamala, Christopher C. Tarver and Peter S. Murano
Affiliation:
Keywords: Colon cancer, functional foods, obesity, Wnt, prostaglandin, IGF, insulin, inflammation
Abstract: Obesity is rapidly becoming a global phenomenon. This is more than a cosmetic issue as obesity is associated with several life-threatening diseases, including colon cancer. Insulin resistance and inflammation, underlying factors in obesity-related diseases, promote colonocyte proliferation and suppress programmed cell death, or apoptosis, by activating the insulin-like growth factor (IGF) and prostaglandin pathways. These pathways converge on the Wnt pathway, which is implicated in colon carcinogenesis. Despite tremendous advances in our understanding of the molecular mechanisms involved in colon carcinogenesis, mortality due to colon cancer world-wide is unacceptably high. Even though conventional therapies can prolong a patients life-span a few years, they cause serious side effects. Thus, there is growing interest in functional foods and dietary bioactive compounds with chemopreventive properties. This search is fueled by the epidemiological studies indicating that plant-based diets are protective against several types of cancers. This review provides a brief summary of the IGF and prostaglandin pathways, which are implicated in obesity-enhanced colon cancer, and some of the functional foods/dietary compounds that target these pathways. It is essential to understand the molecular mechanisms involved in chemoprevention before providing appropriate science-based dietary recommendations to prevent colon cancer in both obese and non-obese individuals.
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Cite this article as:
Vanamala Jairam, Tarver C. Christopher and Murano S. Peter, Obesity-Enhanced Colon Cancer: Functional Food Compounds and their Mechanisms of Action, Current Cancer Drug Targets 2008; 8 (7) . https://dx.doi.org/10.2174/156800908786241087
DOI https://dx.doi.org/10.2174/156800908786241087 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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