Vanderbilt University Medical Center
Pran Datta currently focuses his research on the transforming growth factor-ß (TGF-ß) signal transduction pathways and the role of the molecules involved in these pathways in tumor suppression and promotion.
Dr. Datta received both the Bachelor of Science (1979) in Chemistry and the Master of Science degree (1982) in Organic Chemistry from the University of Burdwan, India. He received the Ph.D. in Organic Chemistry in 1987 from the Bose Institute in Calcutta, where he was a Junior and a Senior Research Fellow, and a Research Scientist, before coming to the United States.
Dr. Datta was appointed as Research Assistant Professor in the Division of Surgical Oncology at Vanderbilt, after completing a postdoctoral research fellowship in 2000 under Dr. Harold Moses' mentorship in the Vanderbilt Cancer Center. He also was a postdoctoral Research Associate at the University of Illinois at Chicago before coming to Vanderbilt in 1995.
Research: Transforming Growth Factor ß Signaling and Gastrointestinal Cancer
"Members of the TGF-ß family regulate a wide range of biological processes including cellular proliferation, cell migration, differentiation, apoptosis, and extracellular matrix deposition. The research in my laboratory focuses on the transforming growth factor-ß (TGF-ß) signal transduction pathways and the role of the molecules involved in these pathways in tumor suppression and promotion. Recently, we have cloned a novel WD-40 domain containing protein, called STRAP (Serine Threonine Kinase Receptor Associated Protein), that associates with both TGF-ß type I receptor (TßRI) and type II receptor (TßRII). STRAP is involved in the negative regulation of TGF-ß signaling. STRAP synergizes with Smad7, an inhibitory Smad, in the inhibition of TGF-ß-induced transcriptional responses. STRAP activates MAPK/ERK pathway, and C-terminus of STRAP is required for binding with two phospho-proteins. Our long-term objective of this line of investigation is (1) to understand the role of STRAP in TGF-ß signaling and (2) to determine how this protein is involved in the crosstalk between TGF-ß and other signaling cascades.
"We have observed that STRAP is upregulated in 45% of breast cancers and in around 70% of colorectal cancers. STRAP induces anchorage-independent growth and enhances tumorigenicity in nude mice. Overexpression of Smad7 in cell culture model blocks TGF-ß signaling and promotes cell proliferation. The expression of Smad7 is increased in human pancreatic cancer. The current studies address the following issues: (1) to determine the role of STRAP and Smad7 in cellular proliferation and tumorigenicity. (2) to study the contribution of functional synergy between STRAP and Smad7 in the progression of colorectal cancers. Blocking the synergistic inhibition of TGF-ß tumor suppressor function by STRAP and Smad7 can be used for the development of successful therapeutic strategies. (3) to study the effect of blocking TGF-ß signals in the intestine by conditionally knocking out TßRII. This aim will be investigated using transgenic mice that carry a floxed TGF-ß RII gene.
"We are involved in teaching and training medical students and surgical residents regarding their research. We are collaborating with clinicians in the Surgical Oncology Division in different field of research, which fits into the goals of the division."
Pran Datta, Ph.D.
Review some of Dr. Datta's abstracts on PubMed.
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