Overexpression of DUXAP9 significantly promotes OSCC cell proliferation, migration, invasion, and xenograft tumor growth and metastasis, and upregulates N‐cadherin, Vimentin, Ki67, PCNA, and EZH2 expression and downregulates E‐cadherin in vitro and in vivo, whereas knockdown of DUXAP9 remarkably suppresses OSCC cell proliferation, migration, invasion, and xenograft tumor growth in vitro and in vivo in an EZH2‐dependent manner. The gene discussed is VIM; the disease is neoplasm.