饮食预防癌症-猫眼课题宝

饮食预防癌症

批准号：

7405370

负责人：

Shrikant Anant

金额：

$27.43万

依托单位：

UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR

依托单位国家：

美国

项目类别：

财政年份：

2005

资助国家：

美国

项目状态：

已结题

起止时间：

2005-07-01 至 2009-04-30

来源：

https://reporter.nih.gov/project-details/7405370

关键词：

1-Phosphatidylinositol 3-Kinase AKT inhibition Adenocarcinoma Affect Angiogenic Factor Apoptosis Apoptosis Promoter Apoptotic Azoxymethane BAX gene Bax protein Biochemical Cause of Death Cell Proliferation Cell Survival Colon Colon Carcinoma Colonic Adenoma Cultured Cells Curcumin Development Diet Dinoprostone Disease Drug Delivery Systems Drug resistance EGF gene Effectiveness End Point Epidermal Growth Factor Epidermal Growth Factor Receptor Food Supplements Gene Targeting Genus Cola Goals Growth Growth Factor Human Hypoxia In Vitro Incidence Intestines Ligands MAPK14 gene MAPK8 gene Malignant Neoplasms Matrix Metalloproteinases Mediating Methods Molecular Mus Neoplasm Metastasis Nude Mice Pathway interactions Pharmaceutical Preparations Phosphorylation Phosphotransferases Population Preventive Process Prostaglandins Prostaglandins E Protein Kinase Protein Tyrosine Kinase Protein p53 Proto-Oncogene Proteins c-akt Rattus Receptor Protein-Tyrosine Kinases Regulation Resistance Risk Role Signal Pathway Signal Transduction Solid Neoplasm Source Specificity Spices Staging TP53 gene Therapeutic Tumeric Tumor Angiogenesis Tumor Biology Tumor Suppressor Proteins United States Vascular Endothelial Growth Factors adenoma angiogenesis cancer cell cancer prevention chemotherapeutic agent chemotherapy clinical phenotype colon cancer cell line cyclooxygenase 2 dietary constituent dietary supplements genetic manipulation in vivo insight irinotecan microbial alkaline proteinase inhibitor migration mutant neoplastic cell neovascularization novel oncoprotein p21 polyphenol prevent receptor response transcription factor tumor tumor progression tumorigenesis

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DESCRIPTION (provided by applicant): Colon Cancer is a leading cause of death in the United States. Accordingly, methods of preventing this disease or discovery of agents that increase effectiveness of existing chemotherapeutic agents would be very beneficial. Our studies and those of others have indicated that dietary curcumin, an active ingredient in the spice turmeric, potently inhibits intestinal tumorigenesis. We have now characterized the mechanisms by which curcumin modulates this function. Proliferation, angiogenesis and tumor invasiveness constitute the major pathways that are necessary for the growth and metastatic potential of cancer. Our preliminary studies show that curcumin inhibits cell proliferation, and tumor angiogenesis and invasiveness, while it enhances spontaneous and chemotherapy-induced apoptosis of tumor cells. The goals of the current project are to determine the mechanistic effects of curcumin on each of theses processes. Specifically, we will determine the effects of curcumin on growth factor-mediated activation of cellular signaling pathways. We will also determine the role of curcumin in signaling mediated by epidermal growth factor and prostaglandins, two molecules that are active in cancer progression. In addition, we will determine the effect of curcumin on the expression and regulation of tumor suppressor protein p53, an important regulator of cell survival. We will examine the effect of curcumin on expression of p53 target genes such as p21 WAF1, BAX. Moreover, we will examine the role of curcumin in the expression of VEGF and related angiogenesis factors as well as matrix metalloproteinases as regulators of tumor invasiveness. We will compare the results obtained in cell culture studies with that observed in mice with defined genetic manipulations. Together these studies should provide insight into the cancer process and how curcumin suppresses the risk and proliferation of colon cancer, and of no less importance, why curcumin is of great value as a food supplement.

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