Rebecca Oberley-Deegan

Assistant Professor, Biochemistry and Molecular Biology 

Rebecca Oberley-DeeganPhone: 402-559-9364 (Office)
    Location: BCC 6.12.391
Fax: 402-559-6650
Email

Education/Training:
B.A. Grinnell College, Grinnell, Iowa - 1999
Ph.D. University of Iowa, Iowa City Iowa - 2004
Postdoctoral training at National Jewish Health, Denver, CO

Research Opportunities in my laboratory:
Not currently accepting graduate students and or MD/PhD students

Research:
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.

Research:
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 has just started phase I clinical trials as a radio-protector to be used in combination with radiation therapy for the treatment of cancer.

Selected Publications:

Chatterjee, A Kosmacek, E.A., Oberley-Deegan, R.E., Manganese treatment or NOX4 inhibition protects radiation-induced damage in mouse primary prostate fibroblasts by inhibiting the TGFB1 signaling pathway. Radiation Research Journal. 2017. Feb 22. doi: 10.1667/RR14623.1.

Tong, Q., Zhu, Y., Galaske, J.W., Kosmacek, E.A., Chatterjee, A., Dickinson, B.C., and Oberley-Deegan, R.E. MnTE-2-PyP modulates thiol oxidation in a hydrogen peroxide-mediated manner in a prostate cancer cell. Free Radical Biology Medicine. 2016, Sep 24;101:32-43.

Stover, K, Fukuyama, T, Oberley, R, Crapo, JD, and Baumer W. Topically applied manganese-porphyrins BMX-001 and BMX-010 display a significant anti-inflammatory response in a mouse model of allergic dermatitis. Arch.Dermatol.Res.2016 Oct 5.

Kosmacek, EA, Chatterjee, A., Tong, Q., Lin, C. and Oberley-Deegan, RE. MnTnBuOE-2-PyP protects normal colorectal fibroblasts from radiation damage and simultaneously enhances radio/chemotherapeutic killing of colorectal cancer cells. Oncotarget.2016 Apr 22.doi:10.18632/oncotarget.8923.

Tong, Q, Weaver MR, Kosmacek EA, O’Connor B, Harmacek L, Venkataraman S, and Oberley-Deegan RE, MnTE-2-PyP reduces prostate cancer growth and metastasis by suppressing p300 activity and p300/HIF-1/CREB binding to the promoter region of the PAI-1 gene.2016. Free Radical Biology Medicine March 2;94.185-194.

Current grants:

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