ArticleNeoplasia (New York, N.Y.)2022
Myeloperoxidase exerts anti-tumor activity in glioma after radiotherapy.
Article in Neoplasia (New York, N.Y.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Myeloperoxidase-DNA complex: a marker and combined target for Pseudomonas aeruginosa-associated bronchiectasis.AMB Express · 2026Article
- Radiomics and clinical data predict pseudoprogression after radiotherapy in high-grade glioma.Frontiers in oncology · 2026Article
- Review
- Passive physical barrier modulates UVB-induced METosis-related MPO expression and activity, 25-hydroxyvitamin D3-1alpha-hydroxylase, and the shift of tissue-resident macrophages toward M1-associated iNOS.Frontiers in immunology · 2025Article
- Neutrophil Extracellular Traps in Tumors and Potential Use of Traditional Herbal Medicine Formulations for Its Regulation.International journal of nanomedicine · 2024Review
- Radiotherapy remodels the tumor microenvironment for enhancing immunotherapeutic sensitivity.Cell death & disease · 2023Review
- Prognosis and immunoinfiltration analysis of angiogene-related genes in grade 4 diffuse gliomas.Aging · 2023Article
- Anticancer and antimicrobial evaluation of extract from brown algae Hormophysa cuneiformis.Journal of applied biomedicine · 2023Article
- Gold nanoparticles enhances radiosensitivity in glioma cells by inhibiting TRAF6/NF-κB induced CCL2 expression.Heliyon · 2023Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundHost immune response is a critical component in tumorigenesis and immune escape. Radiation is widely used for glioblastoma (GBM) and can induce marked tissue inflammation and substantially alter host immune response. However, the role of myeloperoxidase (MPO), a key enzyme in inflammation and host immune response, in tumorigenesis after radiotherapy is unclear. In this study, we aimed to determine how post-radiation MPO activity influences GBM and outcome.
methodsWe injected C57BL/6J or MPO-knockout mice with 005 mouse GBM stem cells intracranially. To observe MPO's effects on post-radiation tumor progression, we then irradiated the head with 10 Gy unfractionated and treated the mice with a specific MPO inhibitor, 4-aminobenzoic acid hydrazide (ABAH), or vehicle as control. We performed semi-quantitative longitudinal molecular MRI, enzymatic assays and flow cytometry to assess changes in inflammatory response and tumor size, and tracked survival. We also performed cell culture experiments in murine and human GBM cells to determine the effect of MPO on these cells.
resultsBrain irradiation increased the number of monocytes/macrophages and neutrophils, and boosted MPO activity by ten-fold in the glioma microenvironment. However, MPO inhibition dampened radiation-induced inflammation, demonstrating decreased MPO-specific signal on molecular MRI and attenuated neutrophil and inflammatory monocyte/macrophage recruitment to the glioma. Compared to saline-treated mice, both ABAH-treated and MPO-knockout mice had accelerated tumor growth and reduced survival. We further confirmed that MPO decreased tumor cell viability and proliferation in cell cultures.
conclusionLocal radiation to the brain initiated an acute systemic inflammatory response with increased MPO-carrying cells both in the periphery and the GBM, resulting in increased MPO activity in the tumor microenvironment. Inhibition or absence of MPO activity increased tumor growth and decreased host survival, revealing that elevated MPO activity after radiation has an anti-tumor role.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.