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Cynthia Smas, D.Sc. Associate Professor of Biochemistry and Cancer Biology cynthia.smas@utoledo.edu |
RESEARCH INTERESTS:
The two main research interests in the laboratory are obesity and prostate cancer. Obesity is now at epidemic proportions and is closely linked to comorbidities including heart disease, diabetes, and some types of cancers. In order to better understand and treat obesity we are studying adipogenesis and the molecular biology of the adipocyte and preadipocyte. Adipogenesis occurs throughout the lifespan, with mature adipocytes arising from preadipocyte precursors present in adipose tissue. Adipogenesis is a contributing factor to total adipocyte number and obesity burden. We are identifying novel gene products that show adipose tissue specific expression patterns, hormonal regulation, and protein sequence elements indicative of important roles in adipocyte function. We are characterizing their function in adipocytes and defining their roles in the pathogenesis of obesity and its comorbidities. Given that visceral (i.e. intra-abdominal) adiposity is closely tied to obesity comorbidities we are particulary interested in studying those gene products that shown differential expression in the visceral adipocytes vs. subcutaneous adipocytes.
Prostate cancer is the most frequently diagnosed malignancy in men and androgen ablation therapy is the main course of treatment. In many cases the disease progresses to an androgen-resistant state, for which there are few viable treatment options. Elucidation of the molecular steps of this process may identify novel points of therapeutic intervention. We are studying the role of the inhibitor of DNA binding Id1 and its protein binding partner E12, as well as other members of the helix-loop-helix (HLH) family of transcriptional regulators in the transition to androgen-independent prostate cancer. The incidence and/or course of various cancers has been reported to correlate with obesity, and adipocytes are key cell types present in the tumor microenvironment. We thus anticipate that points of intersection will arise in our adipocyte and cancer biology projects that should allow for the synergistic utilization of our unique research strengths in both of these subject areas.
Member of the mentoring faculty for the Biomedical Sciences Graduate Program (Cancer Biology track and Cardiovascular and Metabolic Disease track).
EDUCATION:
D.Sc. 1994 Harvard University (Nutritional Biochemistry)
M.S. 1985 University of Massachusetts (Biological Sciences)
B.A. 1980 Boston University (Biology)
ACADEMIC APPOINTMENTS:
01/2008- present Associate Professor, Biochemistry and Cancer Biology, University of Toledo College of Medicine, Toledo, OH
01/2007-present Vice Director, Biomedical Sciences Program, Cancer Biology track
09/2000-12/2007 Assistant Professor, Biochemistry and Cancer Biology, Univ. of Toledo College of Medicine (formerly Medical University of Ohio), Toledo, OH
09/1994-08/2000 Postdoctoral Fellow, Division of Nutritional Sciences and Toxicology, University of California, Berkeley, CA
11/1985-07/1987 Research Assistant, Howard Hughes Medical Department of Neurogenetics, Havard Medical School, Boston, MA
09/1983-06/1985 Research and Teaching Assistant, Department of Biological Sciences University of Massachusetts, Lowell, MA
REPRESENTATIVE PUBLICATIONS:
Liu, K., Zhou, S., Kim, J-Y., Tillison, K., Majors, D., Rearick, D., Lee, J.H., Fernandez-Boyanapalli, R.F., Barricklow, K., Houston, M.S., and Smas, C.M. (2009) Functional analysis of FSP27 protein regions for lipid droplet localization, caspase-dependent apoptosis, and dimerization with CIDEA. Am. J. Physiol Endocrinol. Metab., in press.
Kim, J.Y., Lui, K., Zhou, S., Tillison, K., Wu, Y., and Smas, C.M. (2008) Assessment of fat specific protein 27 (FSP27) in the adipocyte lineage suggests a dual role for FSP27 in adipocyte metabolism and cell death. Am. J. Physiol. Endocrinol. Metab., 294:E654-E667.
Wu, Y., and Smas, C.M. (2008) Wdnm1-like, a new adipokine with a role in MMP-2 activation. Am. J. Physiol. Endocrinol. Metab., 295:E205-215.
Wu, Y., Kim, J.Y., Zhou, S. and Smas, C.M. (2008) Differential screening identifies transcripts with depot-dependent expression in white adipose tissues. BMC Genomics, 9:397.
Wu, Y., and Smas, C.M. (2008) Expression and regulation of transcript for the novel transmembrane protein Tmem182 in the adipocyte and muscle lineage. BMC Research Notes, in press.
Kim, J.Y., Tillison, K., Zhou, S., Lee, J.H., Smas, C.M. (2007) Differentiation-Dependent expression of Adhfe1 in adipogenesis. Arch. Biochem. Biophys. 464:100-111.
Kim, J.Y., Tillison, K.S., Zhou, S., Wu, Y., and Smas, C.M. (2007) The major facilitator superfamily member Slc37a2 is a novel macrophage-specific gene selectively expressed in obese white adipose tissue. Am. J. Physiol. Endocrinol. Metab. 293:E110-E120.
Kim, J.Y., Wu, Y., and Smas, C.M. (2007) Characterization of ScAP-23, a new cell line from murine subcutaneous adipose tissue, identifies genes for the molecular definition of preadipocytes. Physiol. Genomics. 31:328-342.
Kim, J.Y., Tillison, K., Lee, J.H., Rearick, D.A., and Smas, C.M. (2006). The adipose tissue triglyceride lapase ATGL/PNPLA2 is downregulated by insulin and TNF-alpha in 3T3-L1 adipocytes and is a target for transactivation by PPARgamma. Am. J. Physiol. Endocrinol. Metab. 291:E115-E127.
Kim, J.Y., Tillison, K., and Smas, C.M. (2005). Cloning, expression, and differentiation-dependent regulation of SMAF1 in adipogenesis. Biochem. Biophys. Res. Commun. 326:36-44.
Moon*, Y.M., Smas*, C.M., Lee*, K. (*equal authorship), Villena, J., Kim, K.H., Yun, E.J. and Sul, H.S. (2002). Mice lacking paternally-expressed Pref-1/Dlk1 display growth retardation and accelerated adiposity. Mol. Cell. Biol. 22:5585-5592.