Steven J. Berberich, PhD
Ph.D.: 1990 Wright State University (M. Leffak)
Postdoctoral: Princeton University (M.D. Cole)
Gene expression profiling experiments performed with MCF7 breast cancer cells where wild-type p53 was reactivated using RNAi knockdown of Hdm2 or HdmX led to our discovery that YPEL3 (Yippee-like-3), a member of a family of putative zinc finger motif coding genes, is a p53-regulated gene (Heminger, Markey et al. 2009).
We recently published that YPEL3 is directly transactivated by p53, that YPEL3 induction is growth suppressive triggering cellular senescence in various tumor and primary cells and that YPEL3 expression is reduced in ovarian tumors through CpG DNA hypermethylation (Kelley, Miller et al. 2010).
Current research is aimed at addressing the following aspects pertaining to YPEL3:
- What is the mechanism by which YPEL3 triggers cellular senescence?
- Development of mouse models and cell based assays to assess whether YPEL3 a tumor suppressor.
- Understanding how YPEL3 is regulated independent of the p53 tumor suppressor.
- Role of p53 family members in YPEL3 expression.
- Determining the role other YPEL family members play in cell growth.
- Kelley, K. D., K. R. Miller, A. Todd, A. R. Kelley, R. Tuttle and S. J. Berberich (2010). "YPEL3, a p53-Regulated Gene that Induces Cellular Senescence." Cancer Res 70(9): 3566-75.
- Berberich, S. J. (2010). "RNAi knockdown of HdmX or Hdm2 leads to new insights into p53 signaling." Cell Cycle9(18): 3640-1.
- Miller, K. R., K. Kelley, R. Tuttle and S. J. Berberich (2010). "HdmX overexpression inhibits oncogene induced cellular senescence." Cell Cycle 9(16): 3376-82.
- Kelley, K. and S.J. Berberich (2011). FHIT gene expression is repressed by mitogenic signaling through the PI3K/AKT/FOXO pathway. Am J Cancer Res, 1(1): p. 62-70.
- Tuttle, R., M. Simond, D. C. Hitch, J. N. Maiorano, M. Hellan, J. Ouellette, P. Termuhlen and S. J. Berberich(2011). "Senescence Associated Gene, YPEL3, is Down-regulated in Human Colon Tumors." Annals of Surgical Oncology, in press.