Abstract: Objective:To investigate the effect of non-receptor protein tyrosine phosphatase, SHP2, on the regulation of IL-6-induced invasiveness of breast cancer cells as well as its molecular mechanism. Methods:Human breast cancer cells, T 47D, were treated with exogenous IL- 6 or infected with IL- 6-expressing lentivirus. Changes in cell morphology were observed, and cell migration and invasion ability were analyzed. Small interference RNA method was used to downregulate the expression of SHP2, a key molecule in IL- 6 path -way. Wound healing and Transwell methods were used to investigate the effect of SHP2 knockdown on cell migration and invasion, and Western blot method was used to examine the changes of Erk1/2 phosphorylation. Results:Upregulation of IL- 6 significantly en-hances migration and invasion of breast cancer cells. IL- 6 induced a significant morphological switch from the epithelial phenotype to the mesenchymal fibroblast phenotype, downregulation of the epithelial marker E-cadherin, and upregulation of mesenchymal mark -er vimentin. Knockdown of SHP 2 inhibited IL- 6-induced epithelial mesenchymal transition and invasiveness. Phosphorylation of Erk 1/2 also decreased in SHP 2-silencing cells. Conclusion: SHP 2 mediates IL- 6-induced epithelial to mesenchymal transition and promotes in -vasiveness of breast cancer cells.