The　forkhead　box　C2　(Foxc2)　protein,　a　member　of　the　forkhead/winged　helix　transcription　factor　family,　is　strongly　expressed　in　developing　embryo　and　is　required　in　various　developmental　processes.　However,　the　precise　function　of　Foxc2　in　osteoblast　differentiation　remains　largely　unknown.　The　present　study　investigated　the　role　of　Foxc2　overexpression　on　osteogenic　and　adipogenic　differentiations.　In　our　experiment,　rabbit　bone　marrow　mesenchymal　stem　cells　(BMSCs)　were　transduced　with　lentiviral　vectors　containing　Foxc2　or　green　fluorescent　protein　(GFP),　and　the　gene　expression　and　biological　activity　of　Foxc2　were　examined　in　vitro.　The　results　showed　that　the　mRNA　and　protein　expressions　of　Foxc2　were　stable　and　high　in　cells　transduced　with　Foxc2　compared　with　those　transduced　with　GFP.　The　overexpression　of　Foxc2　increased　the　mRNA　and　protein　levels　of　COLI,　OCN,　and　OPN;　enhanced　the　activity　of　ALP　after　osteogenic　induction;　and　decreased　the　expression　of　PPAR　gamma-2　and　the　total　droplet　number　after　adipogenic　induction.　In　addition,　Foxc2　enhanced　the　expression　of　beta-catenin,　an　important　modulator　of　osteoblastogenesis.　XAV939,　a　small　molecule　inhibitor　of　the　Wnt-beta-catenin　pathway,　suppressed　Foxc2-mediated　regulation　of　BMSC　differentiation.　These　findings　demonstrate　that　the　overexpression　of　Foxc2　gene　in　BMSCs　may　promote　osteogenic　differentiation　and　inhibit　adipogenic　differentiation,　and　this　effect　can　be　mediated　via　activating　the　canonical　Wnt-beta-catenin　signaling　pathway.