Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 233, Issue 11, Pages 8499-8507Publisher
WILEY
DOI: 10.1002/jcp.26789
Keywords
cancer stem cells (CSCs); E-cadherin; epithelial dysplasia; epithelial cell adhesion molecule (EpCAM; CD326); oral squamous cell carcinoma (OSCC)
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Oral squamous cell carcinoma (OSCC) is the most common type of head and neck cancer. Epithelial dysplasia is often initiated in the cells and cell nuclei adjacent to the epithelial cell membrane. Reduced cell-cell adhesions enable cancer cells to detach from the tumor and disseminate to other organs. The mutations in epithelial dysplasia markers such as E-cadherin and epithelial cell adhesion molecules (CD326) can lead to proliferation, growth and survival of the tumor cells and persistence of numerous malignancies that play a key role in epithelial dysplasia of OSCC. Accordingly, these genes can be consideredprognostic markers or potential therapeutic targets for the tailored management of patients withOSCC. The gene expression profile of OSCC stem cells indicates a differential pattern that facilitates establishing a cell signature. Owing to the highly tumorigenic behavior of cancer stem cells and the role of these cells in tumor differentiation, treatment resistance, relapse, and metastasis, we reviewed the role of stem cell markers in epithelial dysplasia and OSCC.
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