ArticleJournal of cellular physiology2022
Involvement of Bid in the crosstalk between ferroptotic agent-induced ER stress and TRAIL-induced apoptosis.
Article in Journal of cellular physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- The interaction between endoplasmic reticulum stress and ferroptosis in ovarian diseases.Journal of ovarian research · 2026Pooled it
- The role of ferroptosis in juvenile idiopathic arthritis: Causal inference and mediation by immune phenotypes.Medicine · 2026Article
- Jaceidin Inhibits Proliferation and Promotes Apoptosis in Oral Squamous Cell Carcinoma Cells by Regulating Survivin and AKT/ERK Signaling Pathways.International journal of molecular sciences · 2026Article
- DZ-1-artesunate conjugate induces mitochondria-mediated, reactive oxygen species-dependent apoptosis in colorectal cancer tumoroids.Frontiers in pharmacology · 2026Article
- Tumoricidal Efficacy of Artesunate-Eluting Microsphere-Based Multimodal Therapy in Patient-Derived Colorectal Tumoroids.Biomaterials research · 2026Article
- Ferroptosis in smoke inhalation injury: from mechanisms to potential therapeutic targets.Frontiers in cell and developmental biology · 2026Review
- The efficacy of hyperthermia-based multimodal therapy is dependent on gatekeeper protein, BID.International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group · 2025Article
- Article
- The endoplasmic reticulum stress-ferroptosis reciprocal signaling orchestrates anti-tumor effect of anlotinib in anaplastic thyroid cancer.Cancer cell international · 2025Article
- Ferroptosis in Toxicology: Present and Future.International journal of molecular sciences · 2025Review
- Dioscin pretreatment ameliorates ferroptosis in cardiomyocytes after myocardial infarction via inhibiting endoplasmic reticulum stress.Molecular medicine (Cambridge, Mass.) · 2025Article
- Tumoricidal Efficacy of Artesunate-Eluting Microsphere: Differential Role of Bax/Bak in Orchestration of Cell Death Pathways.Biomaterials research · 2025Article
- Mcl-1 is a Gatekeeper Molecule to Regulate the Crosstalk Between Ferroptotic Agent-Induced ER Stress and TRAIL-Induced Apoptosis.Journal of cellular biochemistry · 2025Article
- Comparative Assessment of Various Formats of TRAIL in Three-Dimensional Cell Culture and Patient-Derived Tumoroids of Colorectal Cancer.Journal of oncology research and therapy · 2025Article
- Multiple entanglements of different cell death pathways, in which caspase-8 and BID interact with cardiolipin*, have been identified.Frontiers in cell and developmental biology · 2025Review
- FAS mediates apoptosis, inflammation, and treatment of pathogen infection.Frontiers in cellular and infection microbiology · 2025Review
- The Role of Ferroptosis in Amyotrophic Lateral Sclerosis Treatment.Neurochemical research · 2024Review
- Neuroprotective effects of anti-TRAIL-ICG nanoagent and its multimodal imaging evaluation in cerebral ischemia-reperfusion injury.Materials today. Bio · 2024Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces death receptor-mediated extrinsic apoptosis, specifically in cancer cells, and Bid (BH3-interacting domain death agonist) plays an important role in TRAIL-induced apoptosis. Ferroptosis is a newly defined form of regulated cell death known to be distinct from other forms of cell death. However, our previous studies have shown that ferroptosis shares common pathways with other types of programmed cell death such as apoptosis. In this study, we investigated the role of Bid in the crosstalk between the ferroptotic agent-induced endoplasmic reticulum (ER) stress response and TRAIL-induced apoptosis. When human colorectal carcinoma HCT116 cells were treated with the ferroptosis-inducing agents artesunate and erastin in combination with TRAIL, TRAIL-induced activation of caspase-8 was enhanced, and subsequently, the truncation of Bid was increased. Similar results were observed when ovarian adenocarcinoma OVCAR-3 cells were treated with the ferroptotic agents in combination with TRAIL. Results from studies with Bid mutants reveal that the truncation of Bid and the presence of intact BH3 domains are critical for synergistic apoptosis. Nonfunctional Bid mutants were not able to activate the mitochondria-dependent apoptosis pathway, which is required for the conversion of p19 to p17, the active form of caspase-3. These results indicate that Bid plays a critical role in the crosstalk between the ferroptotic agent-induced ER stress response and TRAIL-induced apoptosis.
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