Ferroptosis,　a　newly　discovered　form　of　regulated　cell　death,　has　garnered　significant　attention　in　the　field　of　tumor　therapy.　However,　the　presence　of　overexpressed　glutathione　(GSH)　and　insufficient　levels　of　H2O2　in　the　tumor　microenvironment　(TME)　hinders　the　occurrence　of　ferroptosis.　In　response　to　these　challenges,　here　we　have　constructed　the　self-assembled　nanocomplexes　(FeE　NPs)　utilizing　epigallocatechin-3-gallate　(EGCG)　from　green　tea　polyphenols　and　metal　ions　(Fe3+)　as　components.　After　grafting　PEG,　the　nanocomplexes　(FeE@PEG　NPs)　exhibit　good　biocompatibility　and　synergistically　enhanced　tumor-inhibitory　properties.　FeE@PEG　NPs　can　be　disassembled　by　H2O2　in　the　TME,　leading　to　the　rapid　release　of　Fe3+　and　EGCG.　The　released　Fe3+　produces　large　amounts　of　toxic　center　dot　OH　by　the　Fenton　reactions　while　having　minimal　impact　on　normal　cells.　The　generated　center　dot　OH　effectively　induces　lipid　peroxidation,　which　leads　to　ferroptosis　in　tumor　cells.　Meanwhile,　the　released　EGCG　can　autoxidize　to　produce　H2O2,　which　further　promotes　the　production　of　center　dot　OH　radicals　and　increases　lipid　peroxide　levels.　Moreover,　EGCG　also　depletes　the　high　levels　of　intracellular　GSH,　leading　to　an　intracellular　redox　imbalance　and　triggering　ferroptosis.　This　study　provides　new　insights　into　advancing　anticancer　ferroptosis　through　rational　material　design,　offering　promising　avenues　for　future　research.