Associate Professor, Department of Biochemistry and Molecular Biology
PhD, UAMS (Little Rock, Arkansas) 1999
The role of TJs in colorectal cancer progression and metastasis
Majority of the cancer-related deaths result from the cancers of the epithelial origin which include cancers of the colon, prostate, bladder, lung, esophagus, breast, pancreas, ovary, and liver. Although their differentiated properties vary, these tissues are all composed principally of epithelial cells which share similar basic features including polarity and barrier function. So, the question arises: what underlies the differential properties and/or response to the cancer therapy between cancers originated from different epithelial organs irrespective of the similarities among their basic building units and their properties? Notably, cell-cell adhesion weakens or is lost during the process of EMT or as epithelial cells undergo dedifferention. A critical role of E-cadherin, principal constituent of the adherens junction, in the regulation of EMT is known, however it does not help understand the diversity/heterogeneity among the cancers of epithelial origin. This is why recent investigations have explored the status and potential role of the claudin family of tight junction integral proteins in the regulation of cancer process. Notably, outcome have been rewarding as it is suggested that claudin family members may play differential and tissue-specific role in the regulation of carcinogenic process. The claudin family of proteins may hold the potential cue to the heterogeneity among the tumors of epithelial origin and beyond being useful markers may also help provide therapeutic opportunities suited for specific cancer type.
Current Projects in the lab:
- To understand the mechanism of colon cancer progression and metastasis. Our current goal is to understand the molecular mechanisms involved in tight junction/s mediated regulation of colon cancer progression.
- To understand the cross talk of Notch and Wnt/β-catenin signaling and their effect on potential therapeutic options to inhibit claudin-1 deregulation in colon cancer.
- To understand the mechanism of regulation of cell-cell and matrix interaction in colonic homeostasis.
- Develop therapeutic strategies to Treat/prevent Colon Cancer using small molecular inhibitor and natural compounds.
- To understand the role of tight junction protein in triple negative breast cancer.
Research Opportunities in my laboratory:
Graduate students (basic and clinical)
Undergraduate students, summer research
Review some of Dr. Dhawan's abstracts on PubMed.
Claudins and cancer: Fall of the soldiers entrusted to protect the gate and keep the barrier intact.
Singh AB, Dhawan P. Semin Cell Dev Biol. 2015 May 27. pii: S1084-9521(15)00098-1. doi: 10.1016/j.semcdb.2015.05.001. [Epub ahead of print] Review.
Tissue invasion and metastasis: Molecular, biological and clinical perspectives.
Jiang WG, Sanders AJ, Katoh M, Ungefroren H, Gieseler F, Prince M, Thompson SK, Zollo M, Spano D, Dhawan P, Sliva D, Subbarayan PR, Sarkar M, Honoki K, Fujii H, Georgakilas AG, Amedei A, Niccolai E, Amin A, Ashraf SS, Ye L, Helferich WG, Yang X, Boosani CS, Guha G, Ciriolo MR, Aquilano K, Chen S, Azmi AS, Keith WN, Bilsland A, Bhakta D, Halicka D, Nowsheen S, Pantano F, Santini D.
Semin Cancer Biol. 2015 Apr 9. pii: S1044-579X(15)00023-1. doi: 10.1016/j.semcancer.2015.03.008. [Epub ahead of print] Review.
A post-doctoral position is open in Dhawan lab. The post-doctoral fellow is expected to be proficient in molecular biological techniques, will be actively participating in studies using cell culture and transgenic mouse models and tumor related studies. The candidate is also expected to have on hand knowledge of the biochemical techniques including the immune blotting and immunohistochemistry. Selected candidate will work on studies related to colon cancer progression and metastasis".
If interested please contact at email@example.com