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Deanna Edwards, Ph.D.

Assistant Professor, Chen Lab

Research Description

I am working on two projects in the lab.  The overarching goal of the first project is to examine how the EphA2-YAP/TAZ signaling axis regulates glutamine metabolism and glutamine-dependent immunosuppression in breast cancer, primarily HER2-positive and triple-negative breast cancer (TNBC).  The receptor tyrosine kinase EphA2 is commonly overexpressed in breast cancer, particularly in TNBC, leading to increased tumor growth and malignancy while also correlating with reduced overall survival and therapeutic resistance.  We have determined that EphA2 overexpression leads to increased Rho-dependent glutaminolysis, which contributes to tumor growth and progression.  Additionally, we have determined that EphA2 promotes enhanced glutamine uptake and utilization in the cell by regulating expression of the glutamine transporter SLC1A5 and glutaminase (GLS), respectively, through the transcriptional co-activators YAP and TAZ.  This work was recently published in Science Signaling.  Currently, we are examining how tumor-specific glutamine metabolism impacts the tumor microenvironment, particular the infiltration and activation of anti-tumor and pro-tumor immune cells.  We hope to determine if EphA2 may be a novel target to treat patients with TNBC and/or those with metastatic disease.

My second project seeks to identify the role of mTORC2 in several aspects of cancer progression, including tumor cell migration and survival.  Using models of EGFR-mutant non-small cell lung cancer (NSCLC), we have determined that loss of Rictor, the critical component of mTORC2, significantly reduces tumor development in vivo.  Compared to mTORC1, our data suggest that mTORC2 may play a more critical role in the viability of cells resistant to erlotinib, a first generation tyrosine kinase inhibitor (TKI), suggesting that mTORC2 may be a potential target to treat TKI-resistant NSCLC. These findings have been presented at the VICC Annual Scientific Retreat and the VICC Host-Tumor Interactions Program/Department of Cancer Biology Joint Retreat.  We are in the process of finishing a few experiments, and plan on submitting this manuscript for publication in 2018.


Awards and Honors

Susan G. Komen Foundation Postdoctoral Fellowship (PDF17480733), “Targeting the EphA2-YAP/TAZ signaling axis in human breast cancer”, 2017-2020.



Edwards, D. N., Ngwa, V. M., Wang, S., Shiuan, E., Brantley-Sieders, D. M., Kim, L. C., Reynolds, A. B., and J. Chen (2017) The receptor tyrosine kinase EphA2 promotes cancer glutamine metabolism by activating the transcriptional co-activators YAP and TAZ. Sci Signal. 10:eaan4667.  PCMID: 29208682

Youngblood, V. M., Kim, L. C., Edwards, D. N., Hwang, Y., Santapuram, P. R., Stirdivant, S. M., Lu, P., Ye, F., Brantley-Sieders, D. M., and J. Chen (2016) The ephrin-A1/EPHA2 signaling axis regulates glutamine metabolism in HER2-positive breast cancer. Cancer research 76:1825-36, 2016. PCMID: PMC4873477. *These authors contributed equally to this article.