Increasing　evidence　has　demonstrated　the　essential　role　of　inflammatory　micro-environment　in　tumorigenesis　and　tumor　progression.　Some　cancer　cells　in　tumor　maintain　typical　stemness　properties　and,　with　the　capacity　of　self-renewal,　are　thought　to　be　crucial　for　the　initiation　and　maintenance　of　tumors　as　well　as　their　metastasis.　Although　both　inflammatory　micro-environment　and　stemness　properties　played　crucial　roles　in　tumor　initiation　and　development,　currently　it　is　still　unclear　whether　and　how　the　inflammatory　micro-environment　promotes　cancer　stemness　properties.　Here,　we　show　the　first　evidence　that　the　inflammatory　micro-environment　promotes　the　stemness　properties　and　metastatic　potential　of　hepatocellular　carcinoma　(HCC)　via　the　NF-kappa　B/miR-497/SALL4　axis.　We　discover　that　miR-497　directly　targets　SALL4,　negatively　regulates　its　expression,　and　further　inhibits　the　self-renewal　and　metastasis　of　HCC;　more　importantly,　inflammatory　factor　TNF-alpha　inhibits　the　expression　of　miR-497　via　NF-kappa　B-mediated　negative　transcriptional　regulation　and　simultaneously　upregulates　the　expression　of　SALL4　and　promotes　the　self-renewal　and　metastasis　phenotypes　of　HCC　cells.　Moreover,　lower　expression　of　miR-497　is　significantly　associated　with　poor　prognosis　in　HCC　patients.　Taken　together,　our　findings　not　only　revealed　a　novel　signaling　pathway　(NF-kappa　B/miR-497/SALL4　axis)　to　connect　inflammation　with　stemness　properties,　and　clarified　the　molecular　mechanisms　underlying　the　inflammation-mediated　self-renewal　and　metastasis　phenotypes,　but　also　provided　novel　molecular　targets　for　developing　new　anticancer　strategies.