Abstract
The biological function and underlying mechanism of miR-1258 has seldom been investigated in cancer progression, including in oral squamous cell carcinoma (OSCC). In the current study, we revealed that the expression level of miR-1258 was significantly down-regulated in OSCC tissues and cell lines. Restoration of miR-1258 decreased OSCC cell growth and invasion. The luciferase and Western blot assays revealed that SP1 protein was a downstream target of miR-1258. Overexpression of SP1 dismissed miR-1258's effect on cell growth and invasion. We also revealed that c-Myb inhibited miR-1258 by directly binding at its promoter. In addition, miR-1258 inhibited PI3K/AKT and ERK signalling pathway activity. Taken together, these findings demonstrated that miR-1258 may function as a tumour-suppressive micorRNA in OSCC and suggested that miR-1258 may be a potential therapeutic target for OSCC patients.