Background　and　aims:　The　complex　process　of　cancer　metastasis　remains　the　least　understood.　Tumor　cells　alter　their　protein　expression　profile　to　survive　from　the　tumor　metastasis.　Fibronectin　1　(FN1　gene　coding　protein)　is　a　member　of　the　glycoprotein　family　that　has　been　shown　to　play　an　important　role　in　cancer　metastasis.　However,　its　effects　on　melanoma　metastasis　are　still　unclear.　Methods:　We　detected　the　FN1　expression　between　metastatic　cells　and　primary　cells　by　using　Western　blot　and　RT-qPCR　assays.　And,　we　analyzed　the　expressed　feature　of　FN1　in　different　tissues　and　examined　the　clinical　relevance　of　upregulated　FN1　in　melanoma　progression　by　bioinformatic　analysis.　Furthermore,　we　downregulated　the　expression　of　FN1　by　small　interfering　RNA　technique　to　reveal　the　effect　of　FN1　on　melanoma　phenotype　and　expression　of　related　genes.　Finally,　we　used　bioinformatics　to　reveal　the　possible　mechanism　of　FN1　regulating　melanoma　progression.　Results:　We　reported　that　the　expression　of　FN1　was　changed　during　melanoma　metastasis.　In　this　study,　we　established　two　metastatic　cell　lines　of　melanoma　through　mouse　model,　and　found　that　metastatic　cells　exhibited　stronger　mesenchyme　phenotype　and　possessed　higher　FN1　expression　level　compared　to　primary　cells.　Besides,　we　examined　the　clinical　relevance　of　upregulated　FN1　in　tumor　progression.　Small　interfering　RNA　(siRNA)mediated　downregulation　of　FN1　suppressed　the　migration,　invasion,　adhesion,　proliferation　capabilities　and　induced　apoptosis　of　melanoma　cells.　We　detected　a　diminished　EMT-related　gene　signature　including　increased　expression　of　E-cadherin　and　decreased　expression　of　N-cadherin　and　Vimentin.　Downregulation　of　FN1　also　increased　Bax/Bcl-2　ratio　which　might　result　in　apoptosis　of　melanoma　cells.　Bioinformatics　analysis　revealed　that　FN1　most　likely　involved　in　focal　adhesion　and　PI3K-Akt　signaling　pathway　to　regulate　EMT　process　and　apoptosis.　Conclusions:　Taken　together,　these　findings　demonstrated　a　role　of　FN1　in　promoting　melanoma　metastasis　by　inhibiting　apoptosis　and　regulating　EMT.