Using both human OSCC samples and cell lines (UMSCC38 and UMSCC11B), we assessed protein, mRNA, gene expression, and protein–DNA interactions during OSCC progression.
Our results showed that TGF-β1 increased OSCC cell proliferation by upregulating the expression of ΔNp63 and c-Myc oncogenes. Although the basal OSCC cell proliferation is sustained by activating ΔNp63, increased induction of c-Myc causes unregulated OSCC cell proliferation. Following induction of the cell cycle by ΔNp63 and c-Myc, cancer cells that halt c-Myc activity undergo epithelial mesenchymal transition or invasion while those that continue to express ΔNp63/c-Myc undergo unlimited progression through the cell cycle.
OSCC proliferation is manifested by the induction of c-Myc in response to TGF-β1 signaling, which is essential for OSCC growth. Our data highlight the potential role of TGF-β1 in the induction of cancer progression and invasion of OSCC.