Our　previous　study　demonstrated　that　neuroglobin　(Ngb)　functions　as　an　independent　predictive　indicator　of　the　prognosis　of　patients　with　glioma　and　promotes　cancer　cell　growth　by　suppressing　apoptosis.　However,　the　understanding　of　the　mechanisms　underlying　the　survival-enhancing　function　of　Ngb　in　glioma　is　limited.　In　the　present　study,　KEGG　PathwayFinder　by　gene　correlation　analysis　was　performed　on　the　R2:　Genomics　Analysis　and　Visualization　Platform,　which　revealed　a　high　association　between　Ngb　and　the　phosphatidylinositol　3-kinase　(PI3K)/AKT　pathway　using　glioma　data　(GSE4290)　from　the　Gene　Expression　Omnibus　database.　Furthermore,　western　blotting　experiments　were　performed　in　U251　and　U87　glioma　cells,　and　Ngb　knockdown　using　short　hairpin　RNA　reduced　the　protein　levels　of　phosphorylated　(p)-AKT,　p-mammalian　target　of　rapamycin　(mTOR)　and　antiapoptotic　factor　Bcl-2,　and　increased　the　expression　of　the　proapoptotic　protein　Bcl-2-associated　X,　in　U251　cells.　In　addition,　Ngb　overexpression　promoted　the　activation　of　the　PI3K/AKT　pathway　in　U87　cells.　MK2206,　a　PI3K/AKT　signaling　inhibitor,　reduced　the　expression　of　p-AKT　and　increased　the　levels　of　apoptosis-associated　proteins,　including　cleaved　poly(ADP-ribose)　polymerase　1　and　cleaved　caspase-3/7/8,　in　Ngb-overexpressing　U87　cells.　Furthermore,　MK2206　treatment　reduced　the　proliferation　and　induced　the　apoptosis　of　Ngb-overexpressing　U87　cells,　as　indicated　by　the　results　of　MTT,　colony　formation　and　flow　cytometry　assays.　In　addition,　insulin-like　growth　factor-1,　a　PI3K/AKT　signaling　activator,　reversed　Ngb　knockdown-induced　growth　arrest　and　apoptosis　in　U251　cells.　In　conclusion,　the　results　of　the　present　study　indicate　that　Ngb　may　facilitate　a　malignant　phenotype　of　glioma　cells　by　activating　the　PI3K/AKT　pathway.