ArticleLasers in medical science2015
Photodynamic therapy using talaporfin sodium induces concentration-dependent programmed necroptosis in human glioblastoma T98G cells.
Article in Lasers in medical science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 76 citations in OpenAlex.
- Identification and characterization of phyllochlorin sodium as a novel chlorin-derived photosensitiser.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026Article
- Photodynamic therapy using talaporfin sodium for grade 2/3 meningiomas: a preliminary study of safety, feasibility, and clinical outcomes.Journal of neuro-oncology · 2026Article
- Photodynamic therapy for glioblastoma: a narrative review.Journal of neuro-oncology · 2025Review
- Photodynamic Therapy for Glioblastoma: Potential Application of TiOPharmaceutics · 2025Review
- Immunological Insights into Photodynamic Therapy of Glioblastoma Multiforme.Molecules (Basel, Switzerland) · 2025Review
- Phototherapy in cancer treatment: strategies and challenges.Signal transduction and targeted therapy · 2025Review
- Photodynamic therapy and tumor-treating fields therapy for newly diagnosed glioblastoma.Frontiers in oncology · 2025Article
- Necroptosis as a consequence of photodynamic therapy in tumor cells.Lasers in medical science · 2024Review
- Cytocidal Effects of Interstitial Photodynamic Therapy Using Talaporfin Sodium and a Semiconductor Laser in a Rat Intracerebral Glioma Model.Biomedicines · 2024Article
- Efficacy of interstitial photodynamic therapy using talaporfin sodium and a semiconductor laser for a mouse allograft glioma model.Scientific reports · 2024Article
- Induction of ferroptosis by photodynamic therapy and enhancement of antitumor effect with ferroptosis inducers.Journal of gastroenterology · 2024Article
- Near-infrared photodynamic and photothermal co-therapy based on organic small molecular dyes.Journal of nanobiotechnology · 2023Review
- Systematic Review of Photodynamic Therapy in Gliomas.Cancers · 2023Review
- Photodynamic therapy reduces cell viability, migration and triggers necroptosis in prostate tumor cells.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2023Article
- Current Challenges and Opportunities of Photodynamic Therapy against Cancer.Pharmaceutics · 2023Review
- ROS regulation in gliomas: implications for treatment strategies.Frontiers in immunology · 2023Review
- Inhibition of the pseudokinase MLKL alters extracellular vesicle release and reduces tumor growth in glioblastoma.iScience · 2022Article
- Review
- Which cell death modality wins the contest for photodynamic therapy of cancer?Cell death & disease · 2022Review
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Photodynamic therapy (PDT) using photosensitizer induces several types of cell death, such as apoptosis, necrosis, and autophagy, depending on the PDT procedure, photosensitizer type, and cell type. We previously demonstrated that PDT using the photosensitizer talaporfin sodium (mono-L-aspartyl chlorine e6, NPe6; NPe6-PDT) induces both mitochondrial apoptotic and necrotic cell death in human glioblastoma T98G cells. However, details regarding the mechanism of necrosis caused by NPe6-PDT are unclear. Here, we investigated whether or not necroptosis, a recently suggested form of programmed necrosis, is involved in the necrotic cell death of NPe6-PDT-treated T98G cells. Leakage of lactate dehydrogenase (LDH) from the cell layer into conditioned medium was significantly increased by NPe6 (25 and 50 μg/ml)-PDT, indicating that NPe6-PDT induces necrosis in these cells. NPe6 (25 μg/ml)-PDT treatment also induced conversion of microtubule-associated protein 1 light-chain 3 (LC3)-I into phosphatidylethanolamine-conjugated LC3-II accompanying autophagosome formation, indicators of autophagy; however, of note, NPe6 (50 μg/ml)-PDT did not induce such autophagic changes. In addition, both necrostatin-1 (a necroptosis inhibitor) and knockdown of necroptotic pathway-related proteins [e.g., receptor interacting serine-threonine kinase (RIP)-1, RIP-3, and mixed lineage kinase domain-like protein (MLKL)] inhibited leakage of LDH caused by NPe6 (25 μg/ml)-PDT. Taken together, the present findings revealed that NPe6-PDT-induced necrotic cell death is mediated in part by the necroptosis pathway in glioblastoma T98G cells.
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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.