Rebecca Oberley-Deegan

Assistant Professor, Biochemistry and Molecular Biology 

Rebecca Oberley-DeeganPhone: 402-559-9364 (Office)
Fax: 402-559-6650

B.A. Grinnell College, Grinnell, Iowa
Ph.D. University of Iowa, Iowa City Iowa
Postdoctoral training at National Jewish Health, Denver, CO

Research Opportunities in my laboratory:
Currently accepting graduate students and or MD/PhD students

Rebecca Oberley-Deegan’s laboratory has previously shown that a catalytically active antioxidant can protect normal prostate tissues during radiation but not prostate tumor tissues. The focus of her research is determining the mechanisms by which antioxidants can protect normal tissues from radiation while simultaneously making the tumor vulnerable to radiation damage. Dr. Oberley-Deegan’s is focusing specifically on the role of free radical signaling to transform fibroblasts and inflammatory cells in normal tissues, which results in damage to these tissues. In the context of prostate cancer, her group is focusing on inhibiting the signaling events controlled by radiation induced free radicals involved in tumor survival and metastasis. 

Fibrosis and cancer have been described as unsuccessful attempts at wound healing. Both processes begin with the de-differentiation of normal cells, resulting in uncontrolled proliferation and remodeling of the extracellular matrix. Reactive oxygen species (ROS) are thought to be one of the main drivers for both fibrosis and cancer progression. Elevated ROS, through radiation exposure, promotes epigenetic modifications of prostate cancer cells leading to a more aggressive tumor. Radiation also epigenetically modifies normal fibroblasts into myofibroblasts, which results in aberrant extracellular matrix deposition and ultimately causing fibrosis. Dr. Oberley-Deegan’s laboratory is focused on understanding the mechanisms by which ROS promote radiation induced fibrosis and prostate cancer progression.  Her research has shown that scavenging radiation-induced ROS, through the addition of a novel catalytically active antioxidant (MnTE-2-PyP), results in the protection of fibrosis of normal tissues following radiation and enhanced sensitivity of prostate tumors to radiation. In order to determine whether the addition of the ROS scavenger alters epigenetic modifications in the tumor cells, her lab investigated the effects of the antioxidant on histone acetylation. MnTE-2-PyP alters the binding of the p300 (a histone acetyltransferase) protein complex with DNA, which results in reduced acetylation of histone 3 in the promoters of specific genes involved in the progression of prostate cancer. Her laboratory is currently investigating other ways in which ROS scavenging may inhibit radiation induced epigenetic changes in both the tumor and normal tissues following radiation.  This catalytically active antioxidant will soon be entering phase I and phase II clinical trials as a radio-protector to be used in combination with radiation therapy for the treatment of cancer. 

Selected Publications:

Oberley-Deegan, R.E. and J.D. Crapo, Redox-Active Therapeutics, New York, NY Springer US; 2015, Mechanisms by which manganese porphyrins affect signaling in cancer cells.

Pate KM, Sherk VD, Carpenter RD, Weaver MR, Crapo S, Gally F, Chatham LS, Goldstrohm DA, Crapo JD, Kohrt WM, Bowler RP,  Oberley-Deegan RE*, Regan EA*. The beneficial effects of exercise on cartilage are lost in mice with reduced levels of ECSOD in tissues.2015. Journal of Applied Physiology Mar15;118(6):760-7.

Hartney JM, Stidham T, Goldstrohm DA, Oberley-Deegan RE, Weaver MR, Valnickova-Hansen Z, Scavenius C, Denninger RK, Leahy RK, Johnson R, Gally F, Kosmider B, Simmermann AK, Enghild JJ, Nozik-Grayck E and Bowler RP. A common Polymorphism in EC-SOD Affects Cadiopulmonary Disease Risk by altering Protein Distribution. 2014. Circulatory and Cardiovascular Genetics Oct:7(5):659-66.

Oberley-Deegan, R.E., Steffan, J.J, Rove, K.O., Pate, K.M., Weaver, M.R., Spasojevic, I., Frederick, B, Raben, D., Meacham, R.B. Crapo, J.D. and Koul, H.R. The antioxidant, MnTE-2-PyP, prevents side-effects incurred by prostate cancer irradiation. 2012. PLoS One. 7(9): p. e44178.

Jungsuwadee, P., Weaver, M.R., Gally, F., and Oberley-Deegan, R.E. The metalloporpyrin antioxidant, MnTE-2-PyP, inhibits Th2 cell immune responses in an asthma model. 2012. International Journal of Molecular Sciences. 13(8): p. 9785-97.

Current grants:

NIH 1 RO1 CA178888: “MnTE-2-PyP as a radioprotector in prostate cancer therapy”