Accumulating　reports　have　demonstrated　that　long　non-coding　RNAs　(lncRNAs)　play　critical　roles　in　the　occurrence　and　metastasis　of　cholangiocarcinoma　(CCA).　LncRNA　myocardial　infarction　associated　transcript　(MIAT)　has　been　widely　reported　in　hepatocellular　carcinoma,　pancreatic　cancer　and　colorectal　cancer,　but　the　relationship　between　MIAT　and　CCA　progression　has　not　yet　been　investigated.　In　the　present　study,　we　found　that　the　expression　of　MIAT　in　CCA　tissues　was　prominently　higher　than　that　in　normal　bile　duct　tissues.　Moreover,　TCGA-CHOL　data　in　the　GEPIA　platform　further　revealed　the　upregulated　expression　of　MIAT　in　CCA　tissues.　Additionally,　quantitative　real-time　PCR　results　showed　that　MIAT　expression　was　increased　in　CCA　cell　lines　compared　to　the　human　intrahepatic　biliary　epithelial　cell　line.　Functionally,　MIAT　knockdown　significantly　inhibited　cell　proliferation　and　induced　G0/G1　phase　arrest　as　well　as　apoptosis　in　HuCCT-1　and　QBC939　cells.　Conversely,　ectopic　expression　of　MIAT　obviously　facilitated　the　proliferation,　cell　cycle　progression　and　apoptosis　resistance　of　RBE　cells.　Mechanistically,　MIAT　directly　interacted　with　miR-551b-3p　and　inversely　modulated　miR-551-3p　level　in　CCA　cells.　Furthermore,　MIAT　knockdown　reduced　the　expression　of　cyclin　D1　(CCND1),　which　was　rescued　by　miR-551b-3p　silencing　in　HuCCT-1　cells.　Importantly,　CCND1　restoration　partially　reversed　MIAT　knockdown-induced　proliferation　inhibition,　G0/G1　phase　arrest　and　apoptosis　in　HuCCT-1　cells.　In　conclusion,　MIAT　was　frequently　overexpressed　in　CCA.　MIAT　contributed　to　the　growth　of　CCA　cells　by　targeting　miR-551b-3p/CCND1　axis.