Adrienne D Cox

PhD, Associate Professor, UNC-Chapel Hill, Molecular Therapeutics

Adrienne D Cox

Associate Professor
UNC-Chapel Hill
Molecular Therapeutics

31-352 Lineberger Comprehensive Cancer Center
919-966-7712 Lab Phone: 919-966-7711

Clinical profile

Area of interest

Our lab is interested in molecular mechanisms of cancer biology, particularly concerning members of the Ras superfamily of proteins. In our lab, studying the mechanisms whereby mammalian Ras family proteins and their cousins control the conversion of extracellular signals to intracellular responses provides us with several broad areas of experimentation with both basic science and translational bents.

  • Location location location: where small GTPases go and why
  • Disruption of lipid modifications for cancer treatment 
  • Ras and Rho family GTPases: why so many? 
  • Radiation responsiveness: control of death, arrest or survival

One major area of interest is the control of subcellular localization of small GTPases to precise cellular membrane regions.

Another major area of interest is the contribution of novel Rho proteins (Ras homologous) to transformation. Rho proteins represent a highly related family of small GTPases that regulate the actin cytoskeleton, and consequently their most prominent roles include control of cell shape, cell division and motility as well as gene expression. The regulation and functions of the "big three" Rho proteins, Rho, Rac and Cdc42, although the most thoroughly characterized, remain incompletely understood. Why are there so many evolutionarily conserved small GTPases? These Big Three are only the tip of the Rho family iceberg, with several other family members under study in our lab, including Rac3, the Rnd proteins, and Wrch-1 (Wnt-regulated Cdc42 homolog).

Finally, we are trying to understand and then to alter the role of Ras family proteins in cellular responses to ionizing radiation. Irradiated cells must choose between death, arrest and survival. Our ultimate goal is to learn enough about the biology to be able to tip the balance one way for healthy cells and another for cancerous cells. We have begun to dissect the signaling pathways used by Ras and Ras-related oncogenes to confer resistance to radiation. Interestingly, Ras and its cousin R-Ras, both of which are transforming, nevertheless have opposing effects on radiation responses. We have found contributions to Ras-mediated radioresistance from the canonical PI3K/Akt survival pathway, an autocrine pathway involving EGFR family ligands, and a novel Ras/Raf pathway that diverges from Raf/MEK/ERK at the level of MEK. In contrast, R-Ras differentially regulates reactive oxygen species. Our hope is that such studies will someday lead to novel radiosensitizers for cancer treatment.

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