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Advanced Oxidation Nanoprocessing Boosts Immunogenicity of Whole Tumor Cells.

ABSTRACT: Whole tumor cells expressing a wide array of tumor antigens are considered as a highly promising source of antigens for cancer vaccines. However, simultaneously preserving the antigen diversity, improving immunogenicity, and eliminating the potential tumorigenic risk of whole tumor cells are highly challenging. Inspired by the recent progress in sulfate radical-based environmental technology, herein, an advanced oxidation nanoprocessing (AONP) strategy is developed for boosting the immunogenicity of whole tumor cells. The AONP is based on the activation of peroxymonosulfate by ZIF-67 nanocatalysts to produce SO₄ ^-∙ radicals continuously, leading to sustained oxidative damage to tumor cells and consequently extensive cell death. Importantly, AONP causes immunogenic apoptosis as evidenced by the release of a series of characteristic damage associated molecular patterns and at the same time maintains the integrity of cancer cells, which is critical to preserve the cellular components and thus maximize the diversity of antigens. Finally, the immunogenicity of AONP-treated whole tumor cells is evaluated in a prophylactic vaccination model, demonstrating significantly delayed tumor growth and increased survival rate of live tumor-cell-challenged mice. It is expected that the developed AONP strategy would pave the way to develop effective personalized whole tumor cell vaccines in future.

SUBMITTER: Zhang M

PROVIDER: S-EPMC10401122 | biostudies-literature | 2023 Aug

REPOSITORIES: biostudies-literature

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Advanced Oxidation Nanoprocessing Boosts Immunogenicity of Whole Tumor Cells.

Zhang Min M Huang Yiming Y Zou Jie J Yang Yang Y Yao Yue Y Cheng Guofeng G Yang Yannan Y

Advanced science (Weinheim, Baden-Wurttemberg, Germany) 20230521 22

Whole tumor cells expressing a wide array of tumor antigens are considered as a highly promising source of antigens for cancer vaccines. However, simultaneously preserving the antigen diversity, improving immunogenicity, and eliminating the potential tumorigenic risk of whole tumor cells are highly challenging. Inspired by the recent progress in sulfate radical-based environmental technology, herein, an advanced oxidation nanoprocessing (AONP) strategy is developed for boosting the immunogenicit ...[more]

PMID: 37211712

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Project description:LIGHT is a member of the tumor necrosis factor superfamily, which has been claimed to mediate anti-tumor activity on the basis of cancer cures observed in immunocompetent mice bearing transgenic LIGHT-expressing tumors. The preclinical development of a LIGHT-based therapeutic has been hindered by the lack of functional stability exhibited by this protein. Here, we describe the cloning, expression, and characterization of five antibody-LIGHT fusion proteins, directed against the alternatively spliced extra domain A of fibronectin, a conserved tumor-associated antigen. Among the five tested formats, only the sequential fusion of the F8 antibody in single-chain diabody format, followed by the LIGHT homotrimer expressed as a single polypeptide, yielded a protein (termed "F8-LIGHT") that was not prone to aggregation. A quantitative biodistribution analysis in tumor-bearing mice, using radio-iodinated protein preparations, confirmed that F8-LIGHT was able to preferentially accumulate at the tumor site, with a tumor-to-blood ratio of ca. five to one 24 hours after intravenous administration. Tumor therapy experiments, performed in two murine tumor models (CT26 and WEHI-164), featuring different levels of lymphocyte infiltration into the neoplastic mass, revealed that F8-LIGHT could significantly reduce tumor-cell growth and was more potent than a similar fusion protein (KSF-LIGHT), directed against hen egg lysozyme and serving as negative control of irrelevant specificity in the mouse. At a mechanistic level, the activity of F8-LIGHT was mainly due to an intratumoral expansion of natural killer cells, whereas there was no evidence of expansion of CD8 + T cells, neither in the tumor, nor in draining lymph nodes. Abbreviations: CTLA-4: Cytotoxic T-lymphocytes-associated protein 4; EGFR: Epidermal growth factor receptor; HVEM: Herpesvirus entry mediator; IFNγ: Interferon-gamma; LIGHT: Lymphotoxin, exhibits inducible expression and competes with HSV glycoprotein D for binding to herpesvirus entry mediator, a receptor expressed on T lymphocytes; LTβR: Lymphotoxin beta receptor; NF-κB: Nuclear factor "kappa-light-chain-enhancer" of activated B cells; NK: Natural killer cells; PD-1: Programmed cell death protein 1; PD-L1: Programmed death-ligand 1; TNF: Tumor necrosis factor.

Dataset Information

Advanced Oxidation Nanoprocessing Boosts Immunogenicity of Whole Tumor Cells.

Publications

Advanced Oxidation Nanoprocessing Boosts Immunogenicity of Whole Tumor Cells.

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