Background:　The　deregulation　of　E-cadherin　has　been　considered　as　a　leading　cause　of　hepatocellular　carcinoma　(HCC)　metastasis.　BCL6　corepressor-like　1　(BCORL1)　is　a　transcriptional　corepressor　and　contributes　to　the　repression　of　E-cadherin.　However,　the　clinical　significance　of　BCORL1　and　its　role　in　the　metastasis　of　HCC　remain　unknown.　Methods:　Differentially　expressed　BCORL1　between　HCC　and　matched　tumor-adjacent　tissues,　HCC　cell　lines　and　normal　hepatic　cell　line　were　detected　by　Western　blot.　The　expression　of　BCORL1　was　altered　by　siRNAs　or　lentivirus-mediated　vectors.　Transwell　assays　were　performed　to　determine　HCC　cell　invasion　and　migration.　Results:　Increased　expression　of　BCORL1　protein　was　detected　in　HCC　specimens　and　cell　lines.　Clinical　association　analysis　showed　that　BCORL1　protein　was　expressed　at　significant　higher　levels　in　HCC　patients　with　multiple　tumor　nodes,　venous　infiltration　and　advanced　TNM　tumor　stage.　Survival　analysis　indicated　that　high　expression　of　BCORL1　protein　conferred　shorter　overall　survival　(OS)　and　recurrence-free　survival　(RFS)　of　HCC　patients.　Multivariate　Cox　regression　analysis　disclosed　that　BCORL1　expression　was　an　independent　prognostic　marker　for　predicting　survival　of　HCC　patients.　Our　in　vitro　studies　demonstrated　that　BCORL1　prominently　promoted　HCC　cell　migration　and　invasion.　Otherwise,　an　inverse　correlation　between　BCORL1　and　E-cadherin　expression　was　observed　in　HCC　tissues.　BCORL1　inversely　regulated　E-cadherin　abundance　and　subsequently　facilitated　epithelial-mesenchymal　transition　(EMT)　in　HCC　cells.　Notably,　the　effect　of　BCORL1　knockdown　on　HCC　cells　was　abrogated　by　E-cadherin　silencing.　Conclusions:　BCORL1　may　be　a　novel　prognostic　factor　and　promotes　cell　migration　and　invasion　through　E-cadherin　repression-induced　EMT　in　HCC.