Immunotherapy has received widespread attention for its effective and long-term tumor-eliminating ability. However, for immunogenic "cold" tumors, such as prostate cancer (PCa), the low immunogenicity of the tumor itself is a serious obstacle to efficacy. Here, we report a strategy to enhance PCa immunogenicity by triggering cascade self-enhanced ferroptosis in tumor cells, turning the tumor from "cold" to "hot". We developed a transformable self-assembled peptide TEP-FFG-CRApY with alkaline phosphatase (ALP) responsiveness and GPX4 protein targeting. TEP-FFG-CRApY self-assembles into nanoparticles under aqueous conditions and transforms into nanofibers in response to ALP during endosome/lysosome uptake into tumor cells, promoting lysosomal membrane permeabilization (LMP). On the one hand, the released TEP-FFG-CRAY nanofibers targeted GPX4 and selectively degraded the GPX4 protein under the light irradiation, inducing ferroptosis; on the other hand, the large amount of leaked Fe 2+ further cascaded to amplify the ferroptosis through the Fenton reaction. TEP-FFG-CRApY-induced immunogenic ferroptosis improved tumor cell immunogenicity by promoting the maturation of DC cells and increasing intra-tumor T cell infiltration. More importantly, recovered T cells further enhanced ferroptosis by secreting large amounts of IFN-γ. This work provides a novel strategy for the molecular design of synergistic molecularly targeted therapy for immunogenic "cold" tumors. This article is protected by copyright. All rights reserved.