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      Nonferrous Ferroptosis Inducer Manganese Molybdate Nanoparticles to Enhance Tumor Immunotherapy

      Author(s): 1 , 1 , 1 , 2 , 1 , 1 , 3
      Publication date (Electronic):
      Journal: Small
      Publisher: Wiley

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          Abstract

          Tumor immunotherapy is an important tool in oncology treatment. However, only a small percentage of patients have an effective immune response to tumor immunotherapy due to the poor infiltration of pro‐inflammatory immune cells in immune “cold” tumors and an immunosuppressive network in the tumor microenvironment (TME). Ferroptosis has been widely used as a novel strategy to enhance tumor immunotherapy. Herein, manganese molybdate nanoparticles (MnMoOx NPs) depleted the highly expressed glutathione (GSH) in tumors and inhibited glutathione peroxidase 4 (GPX4) expression, thus triggering ferroptosis, inducing immune cell death (ICD), further releasing damage‐associated molecular patterns (DAMPs), and enhancing tumor immunotherapy. Furthermore, MnMoOx NPs can efficiently suppress tumors, promote the maturation of dendritic cells (DCs), infiltrate T cells, and reverse the immunosuppressive microenvironment, making the tumor an immune “hot” tumor. Combination with an immune checkpoint inhibitor (ICI) (α‐PD‐L1) further enhanced the anti‐tumor effect and inhibited metastases as well. The work provides a new idea for the development of nonferrous inducers of ferroptosis to enhance cancer immunotherapy.

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          Lipid peroxidation and ferroptosis: The role of GSH and GPx4.

          Fulvio Ursini, Matilde Maiorino (2020)
          Ferroptosis (FPT) is a form of cell death due to missed control of membrane lipid peroxidation (LPO). According to the axiomatic definition of non-accidental cell death, LPO takes place in a scenario of altered homeostasis. FPT, differently from apoptosis, occurs in the absence of any known specific genetically encoded death pathway or specific agonist, and thus must be rated as a regulated, although not "programmed", death pathway. It follows that LPO is under a homeostatic metabolic control and is only permitted when indispensable constraints are satisfied and the antiperoxidant machinery collapses. The activity of the selenoperoxidase Glutathione Peroxidase 4 (GPx4) is the cornerstone of the antiperoxidant defence. Converging evidence on both mechanism of LPO and GPx4 enzymology indicates that LPO is initiated by alkoxyl radicals produced by ferrous iron from the hydroperoxide derivatives of lipids (LOOH), traces of which are the unavoidable drawback of aerobic metabolism. FPT takes place when a threshold has been exceeded. This occurs when the major conditions are satisfied: i) oxygen metabolism leading to the continuous formation of traces of LOOH from phospholipid-containing polyunsaturated fatty acids; ii) missed enzymatic reduction of LOOH; iii) availability of ferrous iron from the labile iron pool. Although the effectors impacting on homeostasis and leading to FPT in physiological conditions are not known, from the available knowledge on LPO and GPx4 enzymology we propose that it is aerobic life itself that, while supporting bioenergetics, is also a critical requisite of FPT. Yet, when the homeostatic control of the steady state between LOOH formation and reduction is lost, LPO is activated and FPT is executed.
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            Cysteine depletion induces pancreatic tumor ferroptosis in mice

            Michael Badgley, Daniel Kremer, H. Carlo Maurer … (2020)
            Ferroptosis is a form of cell death that results from the catastrophic accumulation of lipid reactive oxygen species (ROS). Oncogenic signaling elevates lipid ROS production in many tumor types and is counteracted by metabolites that are derived from the amino acid cysteine. In this work, we show that the import of oxidized cysteine (cystine) via system x C – is a critical dependency of pancreatic ductal adenocarcinoma (PDAC), which is a leading cause of cancer mortality. PDAC cells used cysteine to synthesize glutathione and coenzyme A, which, together, down-regulated ferroptosis. Studying genetically engineered mice, we found that the deletion of a system x C – subunit, Slc7a11 , induced tumor-selective ferroptosis and inhibited PDAC growth. This was replicated through the administration of cyst(e)inase, a drug that depletes cysteine and cystine, demonstrating a translatable means to induce ferroptosis in PDAC.
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              Designer vaccine nanodiscs for personalized cancer immunotherapy

              Rui Kuai, Lukasz J Ochyl, Keith Bahjat … (2016)
              Despite the tremendous potential of peptide-based cancer vaccines, their efficacy has been limited in humans. Recent innovations in tumor exome sequencing have signaled the new era of personalized immunotherapy with patient-specific neo-antigens, but a general methodology for stimulating strong CD8α+ cytotoxic T-lymphocyte (CTL) responses remains lacking. Here we demonstrate that high density lipoprotein-mimicking nanodiscs coupled with antigen (Ag) peptides and adjuvants can markedly improve Ag/adjuvant co-delivery to lymphoid organs and sustain Ag presentation on dendritic cells. Strikingly, nanodiscs elicited up to 47-fold greater frequencies of neoantigen-specific CTLs than soluble vaccines and even 31-fold greater than perhaps the strongest adjuvant in clinical trials (i.e. CpG in Montanide). Moreover, multi-epitope vaccination generated broad-spectrum T-cell responses that potently inhibited tumor growth. Nanodiscs eliminated established MC-38 and B16F10 tumors when combined with anti-PD-1 and anti-CTLA-4 therapy. These findings represent a new powerful approach for cancer immunotherapy and suggest a general strategy for personalized nanomedicine.
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                Author and article information

                Contributors
                Journal
                Title: Small
                Abbreviated Title: Small
                Publisher: Wiley
                ISSN (Print): 1613-6810
                ISSN (Electronic): 1613-6829
                Publication date Created: November 2023
                Publication date (Electronic): July 07 2023
                Publication date (Print): November 2023
                Volume: 19
                Issue: 45
                Affiliations
                [1 ] Institute of Functional Nano & Soft Materials (FUNSOM) Jiangsu Key Laboratory for Carbon‐Based Functional Materials & Devices Soochow University Suzhou 215123 China
                [2 ] Department of Obstetrics and Gynecology The First Affiliated Hospital of Suzhou University Suzhou 215000 China
                [3 ] Macao Institute of Materials Science and Engineering Macau University of Science and Technology Taipa Macau SAR 999078 China
                Article
                DOI: 10.1002/smll.202303438
                SO-VID: e3187778-1dc1-4e0c-a673-1dd45f29cab1
                Copyright © © 2023
                License:

                http://onlinelibrary.wiley.com/termsAndConditions#vor

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