Hypo-glycosylated E-cadherin promotes mesenchymal-to-epithelial transition in oral squamous cell carcinoma (OSCC) CAL27 cells
Date
2013
DOI
Authors
Tran, Jamie H.
Version
OA Version
Citation
Abstract
Oral squamous cell carcinoma (OSCC) has long been recognized as devastating and is among the most prevalent cancers worldwide. However, the mechanisms responsible for its development and progression remain largely unknown. Three interacting cellular pathways/processes with important roles in cellular metabolism, signaling and intercellular adhesion have been identified to be associated with OSCC and they include the metabolic pathway of protein N-glycosylation, the canonical Wnt signaling pathway and E-cadherin-mediated cell-cell adhesion. Previous studies have shown that N-glycosylation is in an inverse relationship with E-cadherin adhesion, but that it functions in a positive feedback loop with the canonical Wnt signaling pathway. These interactions are dysregulated in OSCC, with aberrantly increased N-glycosylation and canonical Wnt signaling leading to reduced E-cadherin adhesion and increased cell proliferation and migration.
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Description
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Thesis (MSD) --Boston University, Henry M. Goldman School of Dental Medicine, 2013 (Department of Endodontics).
Includes bibliographic reference: leaves 27-29.
Thesis (MSD) --Boston University, Henry M. Goldman School of Dental Medicine, 2013 (Department of Endodontics).
Includes bibliographic reference: leaves 27-29.
License
This work is protected by copyright. Downloading is restricted to the BU community. If you are the author of this work and would like to make it publicly available, please contact open-help@bu.edu.