NATURE . COM {
}
We are analyzing https://www.nature.com/articles/s41420-025-02415-x.
Title:
Ferroptosis: CD8+T cells’ blade to destroy tumor cells or poison for self-destruction | Cell Death Discovery
Description:
Ferroptosis represents an emerging, iron-dependent form of cell death driven by lipid peroxidation. In recent years, it has garnered significant attention in the realm of cancer immunotherapy, particularly in studies involving immune checkpoint inhibitors. This form of cell death not only enhances our comprehension of the tumor microenvironment but is also considered a promising therapeutic strategy to address tumor resistance, investigate immune activation mechanisms, and facilitate the development of cancer vaccines. The combination of immunotherapy with ferroptosis provides innovative targets and fresh perspectives for advancing cancer treatment. Nevertheless, tumor cells appear to possess a wider array of ferroptosis evasion strategies compared to CD8+T cells, which have been conclusively shown to be more vulnerable to ferroptosis. Furthermore, ferroptosis in the TME can create a favorable environment for tumor survival and invasion. Under this premise, both inducing tumor cell ferroptosis and inhibiting T cell ferroptosis will impact antitumor immunity to some extent, and even make the final result run counter to our therapeutic purpose. This paper systematically elucidates the dual-edged sword role of ferroptosis in the antitumor process of T cells, briefly outlining the complexity of ferroptosis within the TME. It explores potential side effects associated with ferroptosis-inducing therapies and critically considers the combined application of ferroptosis-based therapies with ICIs. Furthermore, it highlights the current challenges faced by this combined therapeutic approach and points out future directions for development.
Website Age:
30 years and 10 months (reg. 1994-08-11).
Title:
Ferroptosis: CD8+T cells’ blade to destroy tumor cells or poison for self-destruction | Cell Death Discovery
Description:
Ferroptosis represents an emerging, iron-dependent form of cell death driven by lipid peroxidation. In recent years, it has garnered significant attention in the realm of cancer immunotherapy, particularly in studies involving immune checkpoint inhibitors. This form of cell death not only enhances our comprehension of the tumor microenvironment but is also considered a promising therapeutic strategy to address tumor resistance, investigate immune activation mechanisms, and facilitate the development of cancer vaccines. The combination of immunotherapy with ferroptosis provides innovative targets and fresh perspectives for advancing cancer treatment. Nevertheless, tumor cells appear to possess a wider array of ferroptosis evasion strategies compared to CD8+T cells, which have been conclusively shown to be more vulnerable to ferroptosis. Furthermore, ferroptosis in the TME can create a favorable environment for tumor survival and invasion. Under this premise, both inducing tumor cell ferroptosis and inhibiting T cell ferroptosis will impact antitumor immunity to some extent, and even make the final result run counter to our therapeutic purpose. This paper systematically elucidates the dual-edged sword role of ferroptosis in the antitumor process of T cells, briefly outlining the complexity of ferroptosis within the TME. It explores potential side effects associated with ferroptosis-inducing therapies and critically considers the combined application of ferroptosis-based therapies with ICIs. Furthermore, it highlights the current challenges faced by this combined therapeutic approach and points out future directions for development.
Website Age:
30 years and 10 months (reg. 1994-08-11).
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Keywords {🔍}
cells, ferroptosis, pubmed, article, google, scholar, cancer, tumor, cell, cas, central, immune, cdt, antitumor, lipid, immunotherapy, death, immunity, levels, effects, pathway, chen, peroxidation, treatment, therapy, zhang, expression, function, nature, tme, role, therapeutic, activation, dcs, gpx, wang, ferroptotic, microenvironment, accumulation, activity, resistance, iron, liu, mechanisms, targeting, response, induce, promoting, nat, zhao,
Topics {✒️}
nature portfolio privacy policy open-label keynote-021 study editing long-chain acyl-coa synthetases wnt/β-catenin-mitf pathway advertising unrestrained proliferative nature peroxisome proliferator-activated receptor-gamma barnawi io atf4-chop-chac1 signaling pathway anti-pd-l1 immunotherapy-activated cd8+ pd-1/pd-l1 checkpoint inhibitors social media jama netw open cell-mediated anti-tumor immunity lactate-mediated ampk-scd1 activity reprints middle calcium-independent phospholipase a2β pd-1/pd-l1 bockade dual-edged sword role gcn2-eif2α-atf4 pathway myeloid-derived suppressor cells limiting nf-κb recruitment triple-negative breast cancer nature pd-1/pd-l1 inhibitors significant research gap kras-mutant lung adenocarcinoma jak1-stat1 signaling pathway anti-tumor immune responses mitochondrial iron-sulfur cluster current antitumor research fatty acid oxidation oxidized low-density lipoprotein author information authors small-cell lung cancer important research topic p53-independent tumor suppression image-guided drug delivery jak-stat1-irf1 pathway resist ferroptosis-inducing therapies personal data received official approval ros/acetyl-p53 pathway real-time treatment monitoring inducing epithelial-mesenchymal transformation data protection vhl-defective ccrcc cells
Questions {❓}
- Can tumor cells be specifically induced to undergo ferroptosis without affecting normal antitumor immune cells?
- How can ferroptosis be utilized to reverse the immunosuppressive microenvironment and protect the antitumor effects of immune cells?
- How can we design standardized and reasonable clinical translation experiments based on the atypia and heterogeneity of tumors, and explore reliable biomarkers to predict patients’ responses to ferroptosis-combined immunotherapy?
- How can we minimize the toxic and side effects caused by derivatives of ferroptotic cancer cells?
Schema {🗺️}
WebPage:
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Cell Cycle Analysis
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