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Partha Roy, Ph.D.

Assistant Professor of Bioengineering and Pathology

contact

306 Center for Bioengineering
University of Pittsburgh
300 Technology Drive
Pittsburgh, PA 15219
Email:
Tel: 412-624-7867
Fax: 412-383-8788

Education

Ph. D. (Biomedical Engineering): University of Texas Southwestern Medical Center, Dallas, TX

Post-doc Fellowship (Cell Biology): Harvard Medical School, University of North Carolina, Chapel Hill

Courses Taught

Graduate

Molecular Cell Biology and Biophysics I (BIOE 2520 – Fall semester)
Molecular Cell Biology and Biophysics II (BIOE 2521 –Spring semester)
Graduate Seminar Series (BIOE 2023/24 – Fall and Spring semesters

Undergraduate

Introduction to cell biology-1 (BIOE 1070 – Fall semester)
Introduction to cell biology-2 (BIOE 1071 – Fall semester)

Research

Directed cell migration plays an important role in embryonic development, wound healing, angiogenesis, immune response, cancer invasion and metastasis. Dynamic reorganization of actin cytoskeleton, a key aspect of cell migration, is regulated by the concerted actions of various classes of actin-binding proteins (ABPs). Altered expressions of several ABPs are correlated with aberrant cell motility in pathologic scenarios. One of our main research interests is to study the role of actin-binding proteins in tumor cell invasion and metastasis. Our current effort is focused on profilin-1 (Pfn1), a ubiquitously expressed ABP that is essential for embryonic development and a key molecular regulator for actin dynamics in cells. Interestingly, Pfn1 has also been implicated as a tumor suppressor protein based on its reduced expression in several types of adenocarcinomas (breast, pancreatic, hepatic) and ability to suppress tumorigenicity of breast cancer cells in xenograft models. Utilizing a combination of in vitro and in vivo experimental approaches, we are elucidating the molecular mechanisms underlying a) the tumor suppressive action of Pfn1, and 2) how Pfn1 dysregulation contributes to tumor cell migration, invasion and metastasis. Parallel studies are also conducted to reveal Pfn1’s function in cellular physiology using angiogenesis as a model system. Other research interests in the lab are 1) identifying molecular regulations and novel interacting partners of Pfn1, and 2) studying protein-protein interactions in migrating cells.

Funding Sources

National Cancer Institute (R01-CA108607 – Ongoing)
American Heart Association (0665414U – completed)
Competitive Medical Research Fund (UPMC – completed)
Central Research Development Fund (U. Pittsburgh – completed)

Lab Members

Current
Tuhin Das (Post-doctoral Research Associate)
Zhijie Ding (Graduate Student)
Li Zou (Graduate Student)
Yong Ho Bae (Graduate Student)
William Veon (Graduate Student)
Maria Jaramillo (Graduate Student)
Dave Gau (Undergraduate Researcher)

Alumni
Vaishnavi Panchapakesa (Graduate Student)
Mayur Parepally (Undergraduate Researcher)        
Nitin Narayan (Undergraduate Researcher)             
Andrew Roland (Undergraduate Researcher)
Ted Askar (Undergraduate Researcher)                  
Kunjan Patel (Undergraduate Researcher)
Anna DiRienzo (Undergraduate Researcher)
Bryce Bernard (Undergraduate Researcher)
Richard Jeffries (Undergraduate Researcher)

Selected Publications

  • Bae Y., Ding Z., Zou L., Wells A., Gertler F., Roy P. Loss of Profilin-1 expression enhances breast cancer cell motility by Ena/VASP proteins J of Cell Physiology(IN PRESS)

  • Das T., Bae Y, Wells A., and Roy P (2009). Profilin-1 overexpression upregulates PTEN and suppresses AKT activation in breast cancer cells. J of Cell Physiology(2009) 218(2):436-443.

  • Zou L., Jaramillo M., Whaley D., Wells A., Panchapakesa V., Das T., Roy P.  Profilin-1 is a negative regulator of mammary carcinoma aggressiveness. British Journal of Cancer(2007) 97:1361-1371.

  • Ding Z., Lambrechts A., Parepally M., Roy P. Silencing profilin-1 inhibits endothelial cell proliferation, migration and cord morphogenesis. J. Cell Science (2006) 119:4127-4137.

  • Boukhelifa M., Moza M., Johansson J., Rachlin A., Parast M., Huttelmaie, S., Roy P., Jockusch B. M., Carpen O., Karlsson R., Otey, C. A. The proline-rich protein palladin is a binding partner for profilin. FEBS J. (2006) 273(1):26-33.

  • Humphrey D., Rajfur Z., Imperiali B., Marriott G., Roy P., and Jacobson, K."Application of light-directed activation of caged biomolecules and CALI (chromophore-assisted light inactivation) to problems in cell motility in Live Cell Imaging: A Laboratory Manual (David Spector and Bob Goldman editors)", Cold Spring Harbor Laboratory Press, (2005) pp159-176.

  • Roy P., Jacobson, K. Overexpression of profilin reduces the migration of invasive breast cancer cells. Cell Motility Cytoskel. (2004) 57(2): 84-95.

  • Marriott G., Jacobson K., Roy P. Preparation and light-directed activation of caged proteins. Methods in Enzymol. (Biophotonics). (2003) 360: 274-288.

  • Rajfur Z., Roy P., Otey C., Romer L., Jacobson K. Dissecting the link between stress fibers and focal adhesions by CALI of EGFP-fusion proteins. Nature Cell Biol. (2002) 4(4): 286-293.

  • Roy P., Rajfur Z., Pomorski P., Jacobson K. Microscope-based techniques for studying cell adhesion and migration. Nature Cell Biol. (2002) 4(4): E91-96.

  • Roy P., Rajfur Z., Jones D., Marriott G., Loew L., Jacobson K. Local photorelease of caged-Tb4 in locomoting keratocytes causes cell turning. J. Cell Biol. (2001) 153 (5): 1035-1048.

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