Molecular Mechanisms of Obesity, Inflammation and Cancer: The Use of in vitro Model Approaches for Targeted Prevention Strategies

Jenifer I. Fenton*, 1, 2, Sarah J. McCaskey1, Hillary L. Woodworth1
1 Department of Food Science and Human Nutrition, Michigan State University, East Lansing, MI. 48824, USA
2 The College of Nursing, Michigan State University, East Lansing, MI. 48824, USADepartment of Biotechnology, Faculty of Agro-Industry, Kasetsart University, 50, Chatuchak, Bangkok, 10900, Thailand

© 2010 Fenton et al.

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

* Address correspondence to this author at the Department of Food Science and Human Nutrition, Michigan State University, 208B G.M. Trout Bldg, East Lansing, MI. 48824, USA; Tel: 517-355-8474; Fax: 517-353-8963; Email:


Hormones, growth factors and cytokines produced by adipocytes are associated with cancer progression. We suggest that chronically elevated adipokines as observed in the obese state may have profound effects locally on colon epithelial cells through growth promotion effects, induction of autocrine signaling, angiogenesis and immune cross-talk. This dysregulation of the local environment via a systemic signal may lead to the promotion of colon cancer via a novel set of mechanisms. Elucidating the mechanisms by which obesity may increase cancer risk may lead to the identification of treatment/prevention targets. The use of models of this multistage process should allow for mechanism-based approaches to block phenotypes associated with the process of carcinogenesis. The review highlights using in vitro model systems of these various stages to understand the molecular mechanisms of obesity and cancer risk. The advantage in using these systems is that the response of cells possessing various transformations can be compared to “normal cells”. The key is to identify targets that are aberrant from normal to perturb for cancer prevention strategies. This approach would theoretically reduce the possibility of severe or unwanted side-effects when the target does not also destroy the normal cell mechanisms. Cell models can aid in the identification of those targets and inform rationale translation to animal and human studies.

Keywords: Obesity, adipokine, cancer, colon, prostate, breast, leptin, interleukin-6, adiponectin.