Introduction:　Gliomas　are　the　most　frequent　primary　tumors　in　the　human　brain.　Recent　studies　have　identified　a　class　of　long　noncoding　RNAs,　named　IncRNAs,　which　were　reported　to　participate　in　regulatingthe　development　of　various　diseases,　including　gliomas.　In　our　previous　studies,　we　found　that　IncRNA　UBE2CP3-001　was　overexpressed　in　gliomas　but　not　in　normal　tissue.　However,　the　molecular　functions　of　UBE2CP3-001　in　glioma　are　largely　unknown.　Material　and　methods:　The　presence　of　UBE2CP3-001　in　U87　cells,　glioma　tissues　and　normal　brain　tissues　was　detected　by　real-time　RT-PCR.　The　ability　of　U87　cells　to　migrate　was　analyzed　using　a　cellular　wound　healing　assay　after　downregulation　of　UBE2CP3-001.　The　survival　rate　of　U87　cells　after　UBE2CP3-001　knockdown　was　also　analyzed　using　the　CCK8　assay.　In　vivo　tumor　weights　from　xenograft　tumors　transfected　with　UBE2CP3-001　shRNA　were　further　analyzed　using　in　vivo　animal　experiments.　The　expression　levels　of　MMP-9　and　TRAF3IP2　were　determined　by　Western　blot.　Results:　Our　data　showed　that　UBE2CP3-001　was　overexpressed　in　most　glioma　tissues　(p　＜　0.01).　Downregulation　of　UBE2CP3-001　could　inhibit　cell　migration　(p　＜　0.01)　and　invasiveness　(p　＜　0.01)　of　U87　cells.　Downregulation　of　UBE2CP3-001　in　U87　cells　also　suppressed　the　cell　proliferation　(p　＜　0.01)　and　promoted　apoptosis　(p　＜　0.01).　Furthermore,　in　vivo　studies　confirmed　that　knockdown　of　UBE2CP3-001　could　retard　the　growth　of　U87　xenograft　tumors　(p　＜　0.01).　Western　blot　analysis　showed　that　knockdown　of　UBE2CP3-001　could　effectively　inhibit　the　expression　of　MMP-9　(p　＜　0.01)　and　TRAF3IP2　(p　＜　0.01)　in　U87　glioma　cells.　Conclusions:　These　data　suggest　an　important　role　of　UBE2CP3-001　in　glioma　and　indicate　its　potential　application　in　anti-glioma　therapy.