Differential Gene Expression Profiles of Oral Squamous Cell Carcinomas

Objectives: Oral cancers represent a heterogeneous set of mutations, gene expression profiles, and cellular behaviors resulting in differing rates of proliferation and ability to migrate and metastasize. The primary objective of this study was to evaluate the gene expression profiles of multiple commercially-available oral squamous cell carcinoma (OSCC) lines.
Methods: Total cellular RNA was isolated from the OSCC cell lines SCC-25, SCC-9, and Cal27. After the conversion into cDNA, the expression of 92 genes associated with molecular mechanisms of cancer and 4 endogenous control genes were examined by qRT-PCR. The fold change of gene expression was calculated using the comparative C_T (ΔΔC_T) method.
Results: The expression levels of 92 different genes were compared between the more fibroblast-like SCC-9 cells and the squamous oral cancer cells SCC-25 and Cal27. Eighty-nine percent of the genes examined contained approximately the same expression levels (within a 2-fold range). Five genes (cyclin D3, cyclin dependent kinase inhibitor 1A, integrin subunit beta 1, secreted phosphoprotein 1, and transforming growth factor beta 1) were approximately 10-fold higher in the SCC-9 cells. Five genes (collagen type 1 alpha 1 chain, fibronectin, FYN proto-oncogene, integrin subunit beta 3, and KIT proto-oncogene receptor tyrosine kinase) had dramatically higher expression levels in the SCC-9 cells compared to the SCC-25 and Cal27 cells and ranged from a 40-fold increase to over 1625-fold increase. Only 1 gene, cadherin 1, had substantially less expression and was decreased by 400-fold compared to the SCC-25 and Cal27 cells.
Conclusions: These data strongly suggest that most genes involved in the molecular mechanisms associated with oral cancer were not significantly different. However, the identification of a subset of genes exhibiting altered expression profiles may provide insight into the mechanisms and signaling pathways that are distinct among oral cancers that potentially accounts for differences in oncogenic and metastatic phenotypes.