Cancer, a disease of an uncontrolled cell division, growth and metastasis as a result of genetic mutations, environmental factors and host response, is affecting populations worldwide. Etiology, pathogenicity, and genetics related to cancer are not well understood, and treatment has not been as effective as scientists have expected. Continual research is being done to improve current understanding and treatments. Oral squamous cell carcinoma (OSCC) is one of the most common head and neck cancers (representing >90 % of all head and neck cancers) involving neoplasms of the oral cavity and oropharynx. OSCC is a very pernicious malignancy developed from epithelial cells. There is evidence that a key N-glycosylation gene, DPAGT1, is associated with cancer. Although N-glycosylation of proteins is involved in organ development and homeostasis of tissue, overexpression of DPAGT1 has been implicated in oral cancer initiation and metastasis. Defects in N-glycosylation underlie congenital disorders, while hyper-N-glycosylation has been shown to be a feature of many cancers. The N-glycosylation pathway directs cell adhesion and cytoskeletal dynamics by impacting the function of E-cadherin, a major epithelial cell-cell adhesion receptor. E-cadherin is a tumor suppressor responsible for the organization of multiprotein complexes named adherens junctions (AJs). In epithelial cells, stable AJs are essential for several cellular processes, including inhibition of cell proliferation, reorganization of the actin cytoskeleton, and maintenance of an epithelial phenotype. Indeed, restoration of AJs has been shown to revert cancer cells from a mesenchymal to an epithelial phenotype and to reduce invasiveness. Previous work has shown that upregulation of DPAGT1 plays a pivotal role in driving canonical WNT/β-catenin signaling (also known as canonical Wnt signaling) that represses E-cadherin adhesions and drives tumorigenic phenotypes in oral cancer. This suggests a role in coordinating balance between proliferation and adhesion by DPAGT1. To date, little is known about the molecular and cellular details underlying differences among OSCC cell lines. CAL 27 and HSC-3 are human cancer cell lines commonly used to in laboratory OSCC research. The main differences between these cell lines include capsular tumors formed by CAL27 cells in nude mouse models in contrast to non-capsular and invasive tumors formed by HSC-3 cells. The goal of this study was to characterize biochemical differences between these two cell lines for further research.