The purpose of the present study was to investigate the mechanism by which epigallocatechin?3?gallate (EGCG) inhibits the biological behaviors of the tongue squamous cell carcinoma (TSCC) through the Hippo?tafazzin (TAZ) signaling pathway and to provide insights into molecular targeted therapy in TSCC. CAL27 and SCC15 cells were treated with different concentrations of EGCG for 24?h. Cell proliferation was determined using Cell?Counting Kit?8 and EdU assays. Cell apoptosis was evaluated by flow cytometry. Cell migration and invasion were measured using scratch and Transwell assays, respectively. Furthermore, protein levels of associated target genes were detected using a western blot assay. It was demonstrated that EGCG affected biological behaviors of CAL27 and SCC15 cells in concentration? and time?dependent manners. In addition, EGCG decreased the protein levels of TAZ, LATS1, MOB1 and JNK. Overexpression of TAZ alleviated the effect of EGCG on CAL27 cells. Furthermore, the combination of EGCG and simvastatin inhibited the proliferation, migration and invasion, and promoted apoptosis significantly compared with single treatment in CAL27 cells. The results of the present study suggested that EGCG affects proliferation, apoptosis, migration and invasion of TSCC through the Hippo?TAZ signaling pathway.