ArticleJournal of advanced research2025
Hypericin photoactivation induces triple-negative breast cancer cells pyroptosis by targeting the ROS/CALR/Caspase-3/GSDME pathway.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- KRAS/ERK2-driven stabilization of AARS1 reprograms tumor metabolism and confers Sorafenib resistance in lung adenocarcinoma.Cell death and differentiation · 2026Article
- Article
- Beyond chemotherapy: the evolving role of photodynamic therapy in triple-negative breast cancer.Medical oncology (Northwood, London, England) · 2026Review
- A Study on Traceable Oxygen-Releasing Microspheres in Combination with Bone Marrow Mesenchymal Stem Cells to Enhance Skin Wound Healing.International journal of molecular sciences · 2026Article
- Endoplasmic Reticulum-Targeting NIR Cyanine ER800 Nanoparticles Promote Pyroptosis in Triple-Negative Breast Cancer.ACS applied materials & interfaces · 2026Article
- Cell death pathways and targeting therapeutics in cancer therapy.Acta pharmacologica Sinica · 2026Review
- Feilike and Its Constituent Licochalcone B Trigger Caspase-3/GSDME-Mediated Pyroptosis in Triple-Negative Breast Cancer via Modulation of the Mutant p53-Calcium/ER Stress-ROS-MAPK Axis.Antioxidants (Basel, Switzerland) · 2026Article
- Photo- and Immunotherapy Interface: Can Dendritic Cell Vaccines Overcome the Limitations of PDT?Pharmaceutics · 2026Review
- Hypericin-loaded small extracellular vesicles increase photodynamic therapy and remodel miRNA-mRNA axes in AGS gastric cancer cells.Scientific reports · 2026Article
- Reactive oxygen species (ROS) in cancer: from mechanism to therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Inhibition of LDHA promotes GSDME-dependent pyroptosis by activating RIG-I-like receptor signaling.Apoptosis : an international journal on programmed cell death · 2026Article
- Integrating bulk, single-cell, and spatial transcriptomics to identify a novel pyroptosis-related gene signature for predicting prognosis and tumor immune landscape in triple-negative breast cancer.Frontiers in immunology · 2026Article
- Inflammasome-associated pyroptosis and tumor angiogenesis in prostate cancer.Iranian journal of basic medical sciences · 2026Review
- Hypericin as a Photodynamic Immunomodulator: A Natural Compound for Dermatological Therapy.Drug design, development and therapy · 2026Review
- Platinum-doped emodin carbon dots mitigate sepsis-induced lung injury by targeting the gut-lung axis.Journal of nanobiotechnology · 2025Article
- Amorphous layered double hydroxide-based nano-enzyme eye drops against dry eye disease by inhibiting mitochondrial damage and pyroptosis.Journal of nanobiotechnology · 2025Article
- Developing angiogenesis-related prognostic biomarkers and therapeutic strategies in bladder cancer using deep learning and machine learning.Scientific reports · 2025Article
- Unveiling ammonia-induced cell death: a new frontier in clear cell renal cell carcinoma prognosis.Frontiers in immunology · 2025Article
- Administration of 2-deoxy-D-glucose induces pyroptosis in murine breast cancer cells via cAMP/PKA/HK2 to impair tumor survival.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionHypericin (HP), a natural photosensitizer, has demonstrated great efficacy in photodynamic therapy (PDT) for cancer treatment. In addition to the induction of apoptosis and necrosis through reactive oxygen species (ROS) generation, the therapeutic mechanisms and targets of PDT-HP remain unknown.
objectivesTo investigate the direct targets and mechanisms of action of photoactivated hypericin in the inhibition of triple-negative breast cancer (TNBC).
methodsCell pyroptosis was examined via LDH release, SYTOX Green staining, and ELISA. RNA sequencing, network pharmacology, drug affinity target stability (DARTS)-tandem mass spectrometry (MS/MS), and molecular docking were employed to identify drug targets. Furthermore, immunoblotting and flow cytometry were utilized to elucidate the mechanisms of drug action.
resultsOur research revealed that PDT-HP can induce pyroptosis in TNBC cells. Further investigation revealed that PDT-HP induces endoplasmic reticulum stress, activating Caspase-3 and gasdermin E (GSDME) to trigger TNBC cell pyroptosis. RNA-seq, network pharmacology, and DARTS-MS/MS proteomic analyses revealed that the endoplasmic reticulum protein calreticulin (CALR) is a potential HP target and that interfering with CALR inhibited PDT-HP-induced pyroptosis. During PDT-HP treatment, the interaction between CALR and SERCA2 inactivates SERCA2, increasing the susceptibility of cells to increased intracellular Ca
conclusionIn this study, we provide insight into the antitumor mechanism by examining the pharmacological mechanism by which PDT-HP regulates TNBC cell pyroptosis via the ROS/CALR/Caspase-3/GSDME signaling axis.
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