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Faculty Detail Faculty Entry   
Name DOUGLAS R HURST  
Campus Address VH G019 Zip 0019
Phone 205-934-2951
E-mail dhurst@uab.edu" id="FacultyDetail1EmailAddress"><a href="mailto:dhurst@uab.edu">dhurst@uab.edu</a>
URL
 
 

Department Affiliations(s)
Appointment Type Department Division Rank
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Assistant Professor
Primary  Pathology   Joint Pathology Assistant Professor

Biographical Sketch 
Dr. Hurst received his BS degree from the College of Charleston and his PhD in Biochemistry from the Florida State University where he was a DoD Breast Cancer Research Fellow. He completed postdoc training in Cancer Biology with Danny Welch at the University of Alabama at Birmingham where he was a Ruth L. Kirschstein NIH fellow. He is currently an Assistant Professor in the Department of Pathology.

Society Memberships
Organization Name Position Held Org Link
American Association for Cancer Research  member  http://www.aacr.org/ 
American Association for the Advancement of Science  member  http://www.aaas.org/ 
American Society for Biochemistry and Molecular Biology  member  http://www.asbmb.org/ 
American Society for Matrix Biology  member  http://www.asmb.net/ 
Metastasis Research Society  member  http://www.metastasis-research.org/ 
 

Research/Clinical Interest
Title
Molecular mechanisms of cancer metastasis
Description
Metastasis is the major reason for morbidity and mortality of cancer patients. Therefore, understanding how to effectively target metastasis is vital in order to treat patients with this disease. The molecular mechanisms of metastasis are distinct from the mechanisms regulating growth of the primary tumor and every step of metastasis requires the coordinate expression of specific genetic programs. Several metastasis-associated genes are regulated epigenetically by SIN3:histone deacetylase (HDAC) chromatin remodeling complexes through the recruitment of protein and DNA modifying enzymes. The functional specificity (i.e., which genes they regulate and, as a result, the phenotype that is altered) of these complexes is dictated by their composition and resulting enzyme activity. Our lab focuses on the characterization of the composition and enzyme activity of SIN3:HDAC complexes that regulate chromatin remodeling events important for metastasis to enable the identification of potential targets and a restoration of non-metastatic SIN3:HDAC complexes.

Postdoc Positions Available
Date Posted Position Title
No records
 

Selected Publications 
Publication PUBMEDID
Welch DR and Hurst DR. Unraveling the 'TGF-beta paradox' one metastamir at a time. Breast Cancer Res. 2013;15:305.  23448381 
Hurst DR, Xie Y, Thomas JW, Liu J, Edmonds MD, Stewart MD, Welch DR. The C-Terminal Putative Nuclear Localization Sequence of BReast cancer Metastasis Suppressor 1, BRMS1, Is Necessary for Metastasis Suppression. PLoS One. 2013;8:e55966.  23390556 
Hurst DR. Metastasis suppression by BRMS1 associated with SIN3 chromatin remodeling complexes. Cancer Metastasis Rev. 2012;31:641-51.  22678236 
Frost AR, Hurst DR, Shevde LA, Samant RS. The influence of the cancer microenvironment on the process of metastasis. Int J Breast Cancer. 2012;2012:756257.  22570792 
Cook LM, Cao X, Dowell AE, Debies MT, Edmonds MD, Beck BH, Kesterson RA, Desmond RA, Frost AR, Hurst DR, Welch DR. Ubiquitous Brms1 expression is critical for mammary carcinoma metastasis suppression via promotion of apoptosis. Clin Exp Metastasis. 2012;29:315-25.  22241150 
Ulasov IV, Kaverina NV, Pytel P, Thaci B, Liu F, Hurst DR, Welch DR, Sattar HA, Olopade OI, Baryshnikov AY, Kadagidze ZG, Lesniak MS. Clinical significance of KISS1 protein expression for brain invasion and metastasis. Cancer. 2012;118:2096-2105.  21928364 
Hurst DR and Welch DR. Unraveling the enigmatic complexities of BRMS1-mediated metastasis suppression. FEBS Lett. 2011;585:3185-90.  21827753 
Purushothaman A, Hurst DR, Pisano C, Mizumoto S, Sugahara K, Sanderson RD. Heparanase-mediated loss of nuclear syndecan-1 enhances histone acetyltransferase (HAT) activity to promote expression of genes that drive an aggressive tumor phenotype. J Biol Chem. 2011;286:30377-83.  21757697 
Lee S, Terry D, Hurst DR, Welch DR, Sang QX. Protein Signatures in Human MDA-MB-231 Breast Cancer Cells Indicating a More Invasive Phenotype Following Knockdown of Human Endometase/Matrilysin-2 by siRNA. J Cancer. 2011;2:165-76.  21475635 
Kwon YJ, Hurst DR, Steg AD, Yuan K, Vaidya KS, Welch DR, and Frost AR. Gli1 enhances migration and invasion via up-regulation of MMP-11 and promotes metastasis in ERalpha negative breast cancer cell lines. Clin Exp Metastasis. 2011;28:437-49.  21442356 
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Keywords
metastasis, breast cancer, chromatin remodeling, microenvironment, tumor progression

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