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Faculty Detail    
Name SUSAN L BELLIS
Professor
 
Campus Address MCLM 350A Zip 0005
Phone  (20-5) -441
E-mail  bellis@uab.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor
Secondary  Biomedical Engineering  Biomedical Engineering Associate Professor
Secondary  Cell Biology (Org Ret)  Cell Biology (Org Ret) Associate Professor
Center  Arthritis & Musculoskeletal Diseases Center (Org Ret)  Arthritis & Musculoskeletal Diseases Center (Org Ret) Professor
Center  Biomedical Engineering  Biomatrix Eng Regen Med (BERM) Ctr Professor
Center  Center for Biophysical Sciences/Engineering  Center for Biophysical Sciences/Engineering Professor
Center  Comp Arthritis, MSK, Bone & Autoimmunity Ctr  Comp Arthritis, MSK, Bone & Autoimmunity Ctr Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor
Center  General Clinical Research Center  Ctr for Clinical & Translational Sci Professor
Center  GL Ctr for Craniofacial, Oral, & Dental Disorders  GL Ctr for Craniofacial, Oral, & Dental Disorders Professor
Center  Medicine  Ctr Cardiovasc Bio (Org Ret) Professor
Center  Medicine  Gene Therapy Center Professor
Center  Neurology   Multiple Sclerosis Center Professor
Center  General Clinical Research Center  Nephrology Research & Training Center Professor

Graduate Biomedical Sciences Affiliations
Biochemistry and Structural Biology 
Cancer Biology 
Cell, Molecular, & Developmental Biology 
Immunology 
Integrative Biomedical Sciences 
Medical Scientist Training Program 
Pathobiology and Molecular Medicine 

Biographical Sketch 
I received a Ph.D. in Biochemistry from the University of Rhode Island in 1993, and conducted postdoctoral research at the SUNY Health Science Center in Syracuse, NY. Since starting my laboratory at UAB in 1998, my research program has focused primarily on the role of receptor glycosylation in regulating cell behavior.

Society Memberships
Organization Name Position Held Org Link
American Association for Cancer Research     
Society for Glycobiology     



Research/Clinical Interest
Title
Role of glycosylation in tumor progression and metastasis
Description
The Bellis laboratory is studying the role of receptor glycosylation in regulating tumor cell signaling and phenotype. In particular, we are focused on the ST6Gal-I sialyltransferase, which adds α2-6-linked sialic acids to N-glycosylated proteins. One of our primary research goals has been to identify specific substrates for ST6Gal-I and define the effects of variant sialylation on the structure and function of this cohort. These studies have shown that α2-6 sialylation alters the conformation of the β integrin, driving cell migration and invasion, whereas α2-6 sialylation of the Fas and TNFR1 death receptors prevents receptor internalization, leading to a block in apoptosis. The net effect of elevated tumor cell sialylation is to promote an invasive, apoptosis-resistant cell phenotype. Furthermore, ST6Gal-I imparts all of the hallmark characteristics of a cancer stem cell (CSC) including self-renewal potential, tumor-initiating capability, and resistance to a wide array of cytotoxic stressors including hypoxia, serum-deficiency, chemotherapy drugs and inflammatory stimuli. Furthermore, our group developed the first ST6Gal-I knock-in mouse model and determined that forced ST6Gal-I overexpression drives tumorigenesis in chemically-induced and genetic models of adenocarcinoma. Finally, we have shown that human pancreatic and ovarian cancer tissues have upregulated ST6Gal-I expression, and high ST6Gal-I expression correlates with reduced progression-free and overall patient survival.

Selected Publications 
Publication PUBMEDID
Jones, RB, Hjelmeland, AB, and Bellis, SL. (2018) The ST6Gal-I sialyltransferase protects tumor cells against hypoxia by enhancing HIF-1α signaling. J Biol Chem, 293: 5659-5667    
Holdbrooks, AT, Britain, CM, Bellis, SL. (2018) ST6Gal-I sialyltransferase promotes tumor necrosis factor (TNF)-mediated cancer cell survival via sialylation of the TNF receptor 1 (TNFR1) death receptor. J Biol Chem, 293: 1610-1622   
Chakraborty, A, Dorsett, KA, Trummell, HQ, Yang, ES, Oliver, PG, Bonner, JA, Buchsbaum, DJ, Bellis, SL. (2018) ST6Gal-I sialyltransferase promotes chemoresistance in pancreatic ductal adenocarcinoma by abrogating gemcitabine-mediated DNA damage. J Biol Chem, 293: 984-994    
Britain, CM, Holdbrooks, AT, Anderson JC, Willey, CD, Bellis, SL (2018) Sialylation of EGFR by the ST6Gal-I sialyltransferase promotes EGFR activation and resistance to gefitinib-mediated cell death. J Ovarian Res, 11:12    
Britain, CM, Dorsett, KA, Bellis, SL (2017) The tumor-associated glycosyltransferase ST6Gal-I protects tumor cells against serum growth factor withdrawal by enhancing survival signaling and proliferative potential. J Biol Chem 292: 4663-73   
Schultz, MJ, Holdbrooks, AT, Chakraborty, A, Grizzle, WE, Landen, CN, Buchsbaum, DJ, Conner, MG, Arend, RC, Yoon, K, Klug, CA, Bullard, DC, Kesterson, RA, Oliver, PG, O’Conner, AK, Yoder, BK, Bellis, SL (2016) The tumor-associated glycosyltransferase ST6Gal-I regulates stem cell transcription factors and confers a cancer stem cell phenotype. Cancer Res, 76: 3978-88   

Keywords
tumorigenesis, metastasis, cancer stem cell, cell invasion, apoptosis, tumor immunology,