Abstract
Abstract Introduction: Colorectal cancer affects a large population not only in the United States but worldwide and is one of the major causes of mortality due to cancer. Among the numerous risk factors that might lead to the incidence and development of this disease, inflammatory bowel diseases (IBD) have been identified as a very prominent factor and patients are at much higher risk of developing colorectal cancer in their lifetime. Objective/Hypothesis: As chronic inflammation leads to colorectal cancer and among the various neuromediators, the neuropeptides, particularly neuropeptide Y (NPY) is associated with the development and progression of IBD and as NPY has the potential to augment inflammation and angiogenesis through its Y2 receptor we hypothesize that NPY is an important regulator of the process of development of colorectal cancer (CRC). Results: Our results show that the expression of both NPY its Y2 receptor is upregulated in an axozymethane / dextran sodium sulphate (AOM/DSS) induced mouse model of inflammatory CRC. Upregulation of NPY in AOM/DSS induced CRC in mice is associated with increased angiogenesis. NPY Y2 receptors are expressed in these angiogenic vessels. Furthermore, this upregulation of NPY and Y2 receptor is also related to higher expression of the inflammatory cytokine, TNF-α, that has been shown to promote progression of carcinogenesis in AOM/DSS induced CRC mouse models. Our in vitro studies show that NPY can promote angiogenic potential of human umbilical vein endothelial cells (migration and permeability) through Y2 receptors present in these cells. Conclusion: We here show for the first time that NPY might be associated with the progression of inflammatory colorectal cancer and hence may serve as a prognostic marker of the disease. Citation Format: Chandrani Sarkar, Debanjan Chakroborty. Neuropeptide Y as a prognostic marker of colorectal cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 5354. doi:10.1158/1538-7445.AM2014-5354
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