High　aerobic　glycolysis　not　only　provides　energy　to　breast　cancer　cells,　but　also　supports　their　anabolic　growth.　The　redox　sensitive　transcription　factor　NRF2　is　over-expressed　in　multiple　cancers,　including　breast　cancer.　It　is　unclear　whether　NRF2　could　promote　breast　cancer　cell　growth　through　enhancing　glycolysis.　In　this　study,　we　found　that　NRF2　and　HIF1　alpha　mRNA　and　protein　levels　were　significantly　increased　in　MCF-7　and　MDA-MB-231　breast　cancer　cells　as　compared　to　MCF-10A　benign　breast　epithelial　cells.　Down-regulation　of　NRF2　decreased　MCF7　and　MBA-DA-231　breast　cell　proliferation,　while　it　reversed　by　hypoxia　inducible　factor　1　alpha　(HIF1　alpha).　Knockdown　of　NRF2　inhibited　glycolysis　by　decreasing　the　expression　of　genes　participated　in　glucose　metabolism,　including　HK2,　PFKFB3,　PKM2　and　LDHA.　Our　results　further　indicated　that　the　AKT　activation　and　AMPK　inhibition　were　required　for　NRF2-mediated　up-regulation　of　glycolytic　enzymes.　Consistent　with　these　results,　a　positive　correlation　existed　between　NRF2　or　HIF1　alpha　and　several　key　glycolytic　genes　in　human　breast　cancer　cell　samples　and　breast　cancer　patients　with　high　NRF2　or　HIF1　alpha　expression　had　poorer　overall　survival.　In　conclusion,　our　study　demonstrates　that　NRF2　promotes　breast　cancer　progression　by　enhancing　glycolysis　through　coactivation　of　HIF1　alpha,　implicating　that　NRF2　is　a　potential　molecular　target　for　breast　cancer　treatment.