ArticlePloS one2009
Molecular mechanisms of paraptosis induction: implications for a non-genetically modified tumor vaccine.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 77 citations in OpenAlex.
- Photodynamic therapy mediates antitumor effects through multiple non‑apoptotic cell death pathways.Journal of biomedical science · 2026Review
- Potential therapeutic targeting of BKMolecular oncology · 2026Review
- Paraptosis, a new type of cell death that can be applied to cancer treatment.Frontiers in oncology · 2026Review
- HMGB1: a multifaceted mediator of cell death pathways in cardiovascular diseases.Apoptosis : an international journal on programmed cell death · 2025Review
- Review
- Cytoplasmic Vacuolization: A Fascinating Morphological Alteration From Cellular Stress to Cell Death.Cancer science · 2025Review
- Insights into the Anticancer Mechanisms Modulated by Gamma and Delta Tocotrienols in Colorectal Cancers.Nutrition reviews · 2025Review
- Delayed vacuolation in mammalian cells caused by hypotonicity and ion loss.Scientific reports · 2024Article
- Exploring paraptosis as a therapeutic approach in cancer treatment.Journal of biomedical science · 2024Review
- Natural products-induced cancer cell paraptosis.Food science & nutrition · 2024Article
- Paraptosis-A Distinct Pathway to Cell Death.International journal of molecular sciences · 2024Review
- Targeting paraptosis in cancer: opportunities and challenges.Cancer gene therapy · 2024Review
- TNFRSF19 promotes endoplasmic reticulum stress-induced paraptosis via the activation of the MAPK pathway in triple-negative breast cancer cells.Cancer gene therapy · 2024Article
- Review
- Immunogenic cell death triggered by impaired deubiquitination in multiple myeloma relies on dysregulated type I interferon signaling.Frontiers in immunology · 2023Article
- Recent advances in natural compounds inducing non-apoptotic cell death for anticancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2023Review
- Paraptosis: a unique cell death mode for targeting cancer.Frontiers in pharmacology · 2023Review
- Palmitoylation of Voltage-Gated Ion Channels.International journal of molecular sciences · 2022Review
- Detection of Paraptosis After Photodynamic Therapy.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Glycosylation-Dependent Induction of Programmed Cell Death in Murine Adenocarcinoma Cells.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Paraptosis is the programmed cell death pathway that leads to cellular necrosis. Previously, rodent and human monocytes/macrophages killed glioma cells bearing the membrane macrophage colony stimulating factor (mM-CSF) through paraptosis, but the molecular mechanism of this killing process was never identified. We have demonstrated that paraptosis of rat T9 glioma cells can be initiated through a large potassium channel (BK)-dependent process initiated by reactive oxygen species. Macrophage mediated cytotoxicity upon the mM-CSF expressing T9-C2 cells was not prevented by the addition of the caspase inhibitor, zVAD-fmk. By a combination of fluorescent confocal and electron microscopy, flow cytometry, electrophysiology, pharmacology, and genetic knock-down approaches, we demonstrated that these ion channels control cellular swelling and vacuolization of rat T9 glioma cells. Cell lysis is preceded by a depletion of intracellular ATP. Six-hour exposure to BK channel activation caused T9 cells to over express heat shock proteins (Hsp 60, 70, 90 and gp96). This same treatment forced HMGB1 translocation from the nuclear region to the periphery. These last molecules are "danger signals" that can stimulate immune responses. Similar inductions of mitochondrial swelling and increased Hsp70 and 90 expressions by BK channel activation were observed with the non-immunogenic F98 glioma cells. Rats injected with T9 cells which were killed by prolonged BK channel activation developed immunity against the T9 cells, while the injection of x-irradiated apoptotic T9 cells failed to produce the vaccinating effect. These results are the first to show that glioma cellular death induced by prolonged BK channel activation improves tumor immunogenicity; this treatment reproduces the vaccinating effects of mM-CSF transduced cells. Elucidation of strategies as described in this study may prove quite valuable in the development of clinical immunotherapy against cancer.
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Registered trials
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.