Epigenetic　modifications　such　as　histone　modifications　and　cytosine　hydroxymethylation　are　linked　to　tumorigenesis.　Loss　of　5-hydroxymethylcytosine　(5hmC)　by　ten-eleven　translocation　1　(TET1)　down-regulation　facilitates　tumor　initiation　and　development.　However,　the　mechanisms　by　which　loss　of　TET1　knockdown　promotes　malignancy　development　remains　unclear.　Here,　we　report　that　TET1　knockdown　induced　epithelial-mesenchymal　transition　(EMT)　and　increased　cancer　cell　growth,　migration,　and　invasion　in　DLD1　cells.　Loss　of　TET1　increased　EZH2　expression　and　reduced　UTX-1　expression,　thus　increasing　histone　H3K27　tri-methylation　causing　repression　of　the　target　gene　E-cadherin.　Ectopic　expression　of　the　H3K27　demethylase　UTX-1　or　EZH2　depletion　both　impeded　EZH2　binding　caused　a　loss　of　H3K27　methylation　at　epithelial　gene　E-cadherin　promoter,　thereby　suppressing　EMT　and　tumor　invasion　in　shTET1　cells.　Conversely,　UTX-1　depletion　and　ectopic　expression　of　EZH2　enhanced　EMT　and　tumor　metastasis　in　DLD1　cells.　These　findings　provide　insight　into　the　regulation　of　TET1　and　E-cadherin　and　identify　EZH2　as　a　critical　mediator　of　E-cadherin　repression　and　tumor　progression.