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Indiana University Bloomington

Peter HollenhorstPeter C Hollenhorst

Assistant Professor, Medical Science

Office: Jordan Hall 208


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B.S. 1997 St. Norbert College
Ph.D. 2002 University of Wisconsin
American Cancer Society Postdoctoral Fellow,
Huntsman Cancer Institute, University of Utah


Our lab studies the mechanisms used by sequence specific transcription factors to interact with the genome and regulate gene expression.   The interpretation of genomic sequence by transcription factors allows the proper execution of gene expression programs critical for development and tissue homeostasis.  Because cancer arises when genes are improperly expressed, the mechanisms controlling gene expression are also central to the problem of carcinogenesis.  Our research focuses on understanding mechanisms underlying specific and redundant genomic targeting within a group of 27 human transcription factors called the ETS family.  Chromosomal rearrangements that alter the expression or function of ETS transcription factors occur in a number of different cancer types including approximately one-half of all prostate cancers.  We use techniques ranging from molecular biology and biochemistry to genomics and bioinformatics to understand how ETS transcription factors interact with the human genome to drive normal cell functions, and how this process goes awry in cancer.

 Representative Publications

Selvaraj, N., Kedage, V., and P.C. Hollenhorst (2015). Comparison of MAPK specificity across the ETS transcription factor family identifies a high-affinity ERK interaction required for ERG function in prostate cells. Cell Communication and Signaling 13:12.

Selvaraj, N., Budka, J.A., Ferris, M.W., Plotnik, J.P., and P.C. Hollenhorst (2015). Extracellular signal-regulated kinase signaling regulates the opposing roles of JUN family transcription factors at ETS/AP-1 sites and in cell migration. Molecular and Cellular Biology 35(1): 88-100.

Plotnik, J.P., Budka, J.A., Ferris, M.W., and P.C. Hollenhorst. (2014). ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells. Nucleic Acids Research 42(19): 11928-40.

Selvaraj, N., Budka, J.A., Ferris, M.W., Jerde, T.J., and P.C. Hollenhorst. (2014). Prostate cancer ETS rearrangements switch a cell migration gene expression program from RAS/ERK to PI3K/AKT regulation. Molecular Cancer 13:61.

Foley, J., Nickerson, N., Riese, D.J. 2nd, Hollenhorst, P.C., Lorch, G., and A.M. Foley. (2012). At the crossroads: EGFR and PTHrP signaling in cancer-mediated diseases of the bone. Odontology 100(2): 109-29.

Hollenhorst, P.C., (2012). RAS/ERK pathway transcriptional regulation through ETS/AP-1 binding sites. Small GTPases 1(3).

Hollenhorst, P.C., Ferris, M.W., Hull, M.A., Chae, H., Kim, S., and B.J. Graves. (2011). Oncogenic ETS proteins mimic activated RAS/MAPK signaling in prostate cells. Genes & Development  25(20): 2147-57.

Hollenhorst, P.C., Paul, L., Ferris, M.W., and B.J. Graves.  (2011).  The ETS gene ETV4 is required for anchorage-independent growth and a cell proliferation gene expression program in PC3 prostate cells.  Genes and Cancer 1: 1044-1052.

Hollenhorst, P.C., McIntosh, L.P., and B.J. Graves.  (2011).  Genomic and biochemical insights into the specificity of ETS transcription factors.  Annual Review of Biochemistry 80: 437-71.