Research Program: Genetic Mechanisms of Cancer
Professor, Department of Biochemistry, Molecular Biology, and Biophysics
Distinguished University Teaching Professor

sande001@umn.edu
612-624-9637 — office
612-624-3127 — lab
Preferred method of contact: e-mail

Dr. Sanders received her Ph. D. in Cellular and Molecular Biology in 1981 from the University of Michigan. She conducted postdoctoral research in the laboratory of Dr. G. Stanley McKnight in the Department of Pharmacology at the University of Washington. She joined the University of Minnesota as a faculty member in 1986 and the Masonic Cancer Center in 1997, where she conducts research on the role of estrogen in gene regulation.

Research Interests

Estrogen is an amazing hormone. It drives the proliferation of a number of cell types, regulates reproductive behavior, promotes tissue survival and protects from apoptosis, cardiovascular disease, osteoporosis, diabetes, and dementia. Of course, these beneficial actions of estrogen are mitigated by its positive correlation with reproductive carcinomas in both females and males. As a consequence of the biological importance of estrogen, considerable effort has been expended over the past three decades in defining its detailed mechanism of action.

Our research focuses on investigating how estrogen regulates gene expression, both physiologically and pathologically. One broad area of research is the investigation of the transcriptional regulation of the chick ovalbumin gene. This gene serves as a model to investigate how a secondary response gene is induced by estrogen in a tissue-specific manner. Another major project is the investigation of the role of the estrogen- and androgen-regulated transcription factor ZEB/delta EF1 (ZEB-1) in breast, ovarian, endometrial, and prostate cancers. We have discovered that deregulated expression of ZEB-1 is correlated with rapidly growing, invasive reproductive carcinomas. Experiments are in progress to determine how ZEB-1 contributes to cancer progression and to investigate its mechanism of action. A number of other projects are ongoing that relate to the ability of estrogen to promote cell proliferation and prevent apoptosis (programmed cell death).

Selected Publications

Chamberlain, E. M. and M. M. Sanders (1999). Identification of the novel player deltaEF1 in estrogen transcriptional cascades. Mol Cell Biol. 19:3600-3606.

Monroe, D. G. and M. M. Sanders (2000). Estrogen opposes the apoptotic effects of bone morphogenetic protein 7 on tissue remodeling. Mol Cell Biol. 20:4626-4634.

Park, H-M, S. Ehlen Haecker, S.G. Hagen, and M. M. Sanders (2000). COUP-TF plays a dual role in the regulation of the ovalbumin gene. Biochemistry 39:8537-8545.

Hagen, S. G., D. G. Monroe, D. M. Dean, and M. M. Sanders (2000). Repression of chick multidrug resistance-associated protein 1(ch MRP1) gene expression by estrogen. Gene 257: 243-249.

Dean, D. M., P. S. Jones, and M. M. Sanders (2001). Alterations in chromatin structure are implicated in the activation of the steroid hormone response unit in the ovalbumin gene. DNA Cell Biol. 20:27-39.

Monroe, D. G., R. R. Berger, and M. M. Sanders (2002). Tissue-protective effects of estrogen involve regulation of caspase gene expression. Mol Endocrin. 16:1322-1331.

Dillner, N.B. and M.M. Sanders (2002). Upstream Stimulatory Factor (USF) is recruited into a steroid hormone-triggered regulatory circuit by the estrogen-inducible transcription factor delta EF1. J Biol Chem 277:33890-33894.

Dillner, N. B. and M. M. Sanders. (2004). Transcriptional activation by the zinc finger homeodomain protein deltaEF1 in estrogen signaling cascades. DNA Cell Biol. 23:25-34.

Dougherty, D.C. and M. M. Sanders (2005). Estrogen action: Revitalization of the chick oviduct model. Trends Endocrinol Metab. 16:414-419.