the effects of lncRNA XIST on CRC cell migration and invasion were investigated, along with the interaction between lncRNA XIST and miR-137. LncRNA XIST was upregulated in CRC tissues. Compared with HT29 cells that had low metastatic potential, XIST was markedly higher expressed in LoVo cells that had higher metastatic potential. Overexpression of XIST promoted the migratory and invasive potential of HT29 cells, while knockdown of XIST inhibited the migratory and invasive potential of LoVo cells. Moreover, epithelial-mesenchymal transition (EMT) markers, including Ecadherin, N-cadherin, and Vimentin, exhibited corresponding expression changes. In addition, miR-137 was inhibited by XIST and inhibition of miR-137 could reverse the effects of knockdown of XIST on the migratory and invasive potential of LoVo cells. Furthermore, enhancer of zeste homolog 2 (EZH2) was confirmed as a target of miR-137. Our data reveal that lncRNA XIST may promote tumor metastasis in CRC possible through regulating miR-137-EZH2 axis.