Punita Dhawan

Associate Professor, Department of Biochemistry and Molecular Biology

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402-559-6587 (Office)
402-559-7754 (Lab)
402-559-6650 (Fax)
Email

Education/Training:
PhD, UAMS (Little Rock, Arkansas) 1999

Research:

Identify novel biomarkers and Therapeutics 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:

  1. 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.
  2. To develop novel inhibitors for tight junction proteins for therapeutic implications.
  3. To understand the mechanism of regulation of cell-cell and matrix interaction in colonic homeostasis.
  4. To determine the role of cell cycle protein MASTL in GI cancer and its therapeutic implications using cell, organoid and mouse models.

Research Opportunities in my laboratory:
Graduate students (basic and clinical)
Undergraduate students, summer research

Publications:
My Publications.