REGULATION OF COX-2 IN INTESTINAL NEOPLASIA

COX-2 在肠肿瘤中的调节

• 批准号: 7610472
• 负责人: DAN ALAN DIXON
• 金额: $ 16.43万
• 依托单位: UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-08-01 至 2008-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7610472
• 关键词: Anabolism; Computer Retrieval of Information on Scientific Projects Database; Depth; Development; Epithelial Cells; Funding; Grant; Growth; Inflammatory; Institution; Intestinal Neoplasms; Intestines; Lead; Malignant Neoplasms; Messenger RNA; Mus; PTGS2 gene; Post-Transcriptional Regulation; Prostaglandin-Endoperoxide Synthase; Prostaglandins; Protein Overexpression; RNA-Binding Proteins; Regulation; Research; Research Personnel; Resources; Role; Source; Syndrome; Transcriptional Activation; Transgenic Organisms; Tumorigenicity; United States National Institutes of Health; Up-Regulation; cyclooxygenase 1; cyclooxygenase 2; in vivo; tumor; tumorigenesis

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Dr. Dixon is atudying cyclooxygenases (specifically COX-2), which are central to prostaglandin biosynthesis and are intimately involved in inflammatory syndromes and in cancer. He has shown that HuR, an RNA binding protein that stabilizes COX-2 mRNA through interaction with the latters AU-rich region, is overexpressed in tumors. Dr. Dixon hypothesizes that high HuR levels promote COX-2 overproduction and tumorigenesis. He will determine if up-regulation of HuR leads to enhanced growth and tumorigenicity of cultured epithelial cells. In addition, he will assess the impact of transgenic HuR overproduction on COX-2 levels and tumor development in the mouse intestinal tract in vivo. Dr. Dixons studies should lead to a deeper understanding of the role of post-transcriptional regulation of COX-2 expression in tumor development in the intestinal tract.

这个子项目是许多利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 博士狄克逊正在研究环加氧酶（特别是考克斯-2），它是前列腺素生物合成的中心，与炎症综合征和癌症密切相关。 他已经表明，HuR是一种RNA结合蛋白，通过与考克斯-2 mRNA相互作用来稳定后者。富含AU的区域在肿瘤中过表达。 狄克逊博士假设高水平的HuR促进考克斯-2的过度产生和肿瘤发生。 他将确定HuR的上调是否会导致培养的上皮细胞的生长和致瘤性增强。 此外，他还将评估转基因HuR过量生产对小鼠体内肠道中考克斯-2水平和肿瘤发展的影响。 狄克逊医生的研究将导致对考克斯-2表达的转录后调节在肠道肿瘤发展中的作用有更深的理解。