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dan a. dixon, phd
Assistant Professor, USC, Biological Sciences
Assistant Professor (Adjunct), USC, Pathology and Microbiology
Senior Member, South Carolina Cancer Center
Associate Member, Hollings Cancer Center, Medical University of South Carolina
Degrees
PhD, 1994, Northwestern University
Research Interests
Colon Carcinogenesis, Inflammation, Post-Transcriptional Gene Regulation
Colorectal cancer is the second leading cause of cancer death in the United States, with a yearly mortality rate of ~50,000. Despite advances in the understanding and treatment of colorectal cancer, there is no effective chemopreventive drug for the prevention of colon cancer at its earliest stages. Thus, more effort is needed to improve our understanding of colorectal cancer biology in order to identify new molecular targets and improve upon the current treatment and prevention strategies. The main focus of my research has centered on the molecular mechanisms regulating the expression of the inducible form of cyclooxygenase (COX-2). This enzyme plays a central role in the production of prostaglandins, which are regulators of intestinal epithelial cell growth and proliferation. The expression of COX-2 and associated angiogenic factors are normally tightly regulated on both the transcriptional and post-transcriptional levels. However, constitutive overexpression of these factors plays a key role in colon carcinogenesis and chronic inflammatory syndromes. My laboratory is interested in understanding the functional significance post-transcriptional regulation plays in controlling COX-2 expression and that, if dysregulated, allows for overexpression of COX-2 and other angiogenic factors as detected in disease states. By better understanding the cellular mechanisms involved in regulating cancer-associated gene expression, novel successful therapeutic strategies to prevent neoplastic cell growth and tumorigenesis
will be developed.
Current Research Projects
Regulation of COX-2 Expression in Colorectal Cancer
My primary research has demonstrated that post-transcriptional regulation is an essential mechanism regulating COX-2 gene expression. Loss of post-transcriptional regulation occurs in colon carcinoma cells resulting in constitutive COX-2 and prostaglandin overexpression. Using molecular, cellular, and in vivo approaches, the emphasis of this project is to better understand the cellular defects in COX-2 gene expression that are seen in colorectal neoplasia.
Cellular Adhesion and Signal-Dependent Regulation of COX-2 Expression in Inflammatory Syndromes
Adhesion-dependent signaling plays a key role in the control of leukocyte gene expression in many inflammatory syndromes such as inflammatory bowel disease and atherosclerosis. However, the chronic interaction between leukocytes and platelets allow for enhanced COX-2 protein expression through defects in post-transcriptional regulation. The goal of this research project is to define the signaling mechanisms involved in promoting overexpression of COX-2 seen in states of chronic inflammation and defining the pertinent factors participating in this component of dysregulated gene expression.
Investigation of Anti-Inflammatory Agents that Regulate COX-2 Expression
Increasing evidence suggests that anti-inflammatory cytokines, glucocorticoids, and cytokine specific anti-inflammatory drugs (CSAIDs) downregulate COX-2 expression through post-transcriptional control mechanisms. Characterization of their ability to promote mRNA degradation in neoplastic and inflamed cells is a focus of this project Along with defining the specific molecular mechanisms influenced by these agents, these studies will give insight into potential mechanisms of acquired cellular resistance.
Contact Information
Main Office and Lab:
South Carolina Cancer Center
Division of Basic Research
University of South Carolina
14 Richland Medical Park, Suite 500
Columbia, SC 29203
Dept. Biol. Sci. Office:
Department of Biological Sciences
Room CLS 404
University of South Carolina
Columbia, SC 29208
E-mail
Primary Office: 803.434.3713 | Biology: 803.777.5539
Lab: 803.434.2549 | Fax: 803.434.3795
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