Accumulating　evidence　have　suggested　that　long　non-coding　RNAs　(lncRNAs)　had　malfunctioning　roles　in　the　development　of　human　cancers.　The　present　study　aimed　to　investigate　the　role　of　lncRNA　small　nucleolar　RNA　host　gene　5　(SNHG5)　in　hepatocellular　carcinoma　(HCC)　progression　using　human　tissues　and　cell　lines.　The　quantitative　real-time　PCR　results　showed　that　SNHG5　was　up-regulated　in　both　HCC　tissues　and　hepatoma　cell　lines　and　was　closely　associated　with　tumor　size,　hepatitis　B　virus　infection,　histologic　grade,　TNM　stage,　and　portal　vein　tumor　thrombus　(PVTT)　in　HCC　patients.　Knockdown　of　SNHG5　induced　apoptosis　and　repressed　cell　cycle　progression,　cell　growth,　and　metastasis　in　hepatoma　cell　lines,　whereas　overexpression　of　SNHG5　had　the　opposite　effects.　In　vivo　functional　assay,　xenograft　tumors　grown　from　SNHG5-knockdown　cells　had　smaller　mean　volumes　than　the　tumors　grown　from　negative　control　cells.　Further　investigations　showed　that　SNHG5　may　act　as　a　competing　endogenous　RNA　by　competitively　binding　miR-26a-5p　and　thereby　modulating　the　derepression　of　downstream　target　GSK3　beta,　which　were　further　confirmed　by　luciferase　reporter　assay.　Functionally,　SNHG5　promotes　tumor　growth　and　metastasis　by　activating　Wnt/beta-catenin　pathway　and　inducing　epithelial　to　mesenchymal　transition　(EMT).　Taken　together,　SNHG5　promotes　HCC　progression　by　competitively　binding　miR-26a-5p　and　regulating　GSK3　beta　and　Wnt/beta　catenin　signal　pathway.