DAN A. DIXON

Dan A. Dixon

Associate Professor of Biological Sciences
Cancer Research Center
Ph.D., 1994, Northwestern University
Office: 803-777-4686
Lab: 803-777-4767
ddixon@biol.sc.edu

Dixon Lab
PSC 622

Research Interests:

Post-Transcriptional Gene Regulation in Colorectal Cancer
Colorectal cancers are a leading cause of cancer incidence and death among adult Americans. Commonly observed in colon cancer cells and tumors is overexpression of many growth- and inflammation-associated genes. The overabundance of these factors, which include proto-oncogenes, inflammatory mediators, and angiogenic growth factors, allows the tumor cell to proliferate, promote angiogenesis, escape apoptosis, and metastasize. In normal cells, post-transcriptional mechanisms involving RNA-binding proteins and microRNAs play a critical role by identifying these oncogenic mRNAs and targeting them for rapid decay. Whereas, in tumor cells loss of this critical mechanism is commonly observed allowing for significant oncogenic gene overexpression. By better understanding these post-transcriptional mechanisms, we aim to identify and define new molecular targets for controlling oncogenic gene expression in colorectal cancer and improve on current treatment and prevention strategies.

Role of RNA-Binding Proteins in Cancer
A critical point in controlling the expression of growth- and inflammation-associated genes in normal cells occurs through post-transcriptional mechanisms that regulate mRNA decay. The two primary RNA-binding proteins associated with this are the mRNA stability factor HuR and the mRNA decay factor TTP. Both of these factors bind AU-rich mRNA elements (ARE) present in a majority of cancer-associated mRNAs and target the mRNA for stabilization or rapid decay. However, a common feature observed in various tumor types is the overexpression of the stability factor HuR and loss of expression of the decay factor TTP. These combined defects allow for stabilization and overexpression of cancer-associated growth factors. Current projects involve characterization of the novel tumor promoting function of HuR and tumor suppressing function of TTP. By their ability to control a large number of oncogenic transcripts, we are examining these RNA-binding proteins as therapeutic targets that can counteract the oncogenic effects of mRNA stabilization.

Regulation of COX-2 Expression in Cancer
The inducible prostaglandin synthase COX-2 mediates inflammatory responses and plays a pivotal role in the pathogenesis of several cancer types due to its overexpression. Various studies have demonstrated the chemopreventive effects of COX-2 inhibition using non-steroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors, however concerns related to the unwanted side effects of these drugs have limited their use as anti-cancer compounds. Our research has shown that post-transcriptional regulation is an essential mechanism regulating COX-2 gene expression and loss of this regulation occurs in cancer cells. Using molecular, cellular, and in vivo approaches, we are examining the functional significance post-transcriptional regulation plays in controlling COX-2 expression.

Selected Publications: Click HERE

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