MG53 Inhibits the Progression of Tongue Cancer Cells through Regulating PI3K‐AKT Signaling Pathway: Evidence from 3D Cell Culture and Animal Model

MG53 is transcriptionally activated by the IRS‐1/PI3K/AKT signal pathway, which is closely related with oncogenesis of several tumors. Here, the role of MG53 in the tumorigenesis of tongue cancer is analyzed in vitro and in vivo. The stable MG53 overexpression/knockdown SCC9 and SCC25 cells are constructed through retrovirus infection. Then a PLGA cylinder is used to provide a 3D culture environment for cell growth. Cell counting results suggest that overexpression of MG53 inhibits the cell proliferation and colony formation of SCC9 and SCC25 cells. While knockdown of MG53 has the opposite effect. Furthermore, knockdown of MG53 significantly promotes the invasion of SCC9 and SCC25 cells. Western blotting data confirm that MG53 affects the expression of the AKT signaling pathway. In a xenograft assay, knockdown of MG53 promotes the growth of xenograft which is induced by SCC25 cells in nude mice. The findings demonstrate that MG53 affects the biological behavior of human tongue cancer SCC9 and SCC25 cells. A PLGA cylinder, which provides 3D culture environment for cells, is used to determine the proliferation changes of human tongue cancer SCC9 and SCC25 cells induced by MG53. Knockdown of MG53 not only increases the growth of tongue cancer cells but also promotes their invasive ability. A xenograft assay also reaches the same conclusion.