ArticleInternational journal of molecular sciences2020
Endoplasmic Reticulum Stress Contributes to Indomethacin-Induced Glioma Apoptosis.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Gut Microbiota in NSAID Enteropathy: Current Evidence and Future Perspectives for Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Multi-omics evidence reveals a causal role of endoplasmic reticulum stress in cancer development.PeerJ · 2026Article
- Gene regulatory networks analysis for the discovery of prognostic genes in gliomas.Scientific reports · 2025Article
- Construction of an Extracellular Matrix-Related Risk Model to Analyze the Correlation Between Glioblastoma and Tumor Immunity.BioMed research international · 2025Article
- Endoplasmic reticulum stress-a key guardian in cancer.Cell death discovery · 2024Review
- Cyclooxygenase and Cancer: Fundamental Molecular Investigations.International journal of molecular sciences · 2023Article
- ASK1 inhibitor NQDI‑1 decreases oxidative stress and neuroapoptosis via the ASK1/p38 and JNK signaling pathway in early brain injury after subarachnoid hemorrhage in rats.Molecular medicine reports · 2023Article
- Comprehensive analysis of the biological functions of endoplasmic reticulum stress in prostate cancer.Frontiers in endocrinology · 2023Article
- Endoplasmic Reticulum Stress Contributed to Dipyridamole-Induced Impaired Autophagic Flux and Glioma Apoptosis.International journal of molecular sciences · 2022Article
- Saikosaponin D Inducing Apoptosis and Autophagy through the Activation of Endoplasmic Reticulum Stress in Glioblastoma.BioMed research international · 2022Article
- KDELR2 knockdown synergizes with temozolomide to induce glioma cell apoptosis through the CHOP and JNK/p38 pathways.Translational cancer research · 2021Article
- Novel Applications of NSAIDs: Insight and Future Perspectives in Cardiovascular, Neurodegenerative, Diabetes and Cancer Disease Therapy.International journal of molecular sciences · 2021Review
- Endoplasmic Reticulum Stress Contributes to Gefitinib-Induced Apoptosis in Glioma.International journal of molecular sciences · 2021Article
- Comprehensive Analysis of the Clinical and Biological Significances of Endoplasmic Reticulum Stress in Diffuse Gliomas.Frontiers in cell and developmental biology · 2021Article
- Gut Microbiota in NSAID Enteropathy: New Insights From Inside.Frontiers in cellular and infection microbiology · 2021Review
- S-allyl-L-cysteine protects hepatocytes from indomethacin-induced apoptosis by attenuating endoplasmic reticulum stress.FEBS open bio · 2020Article
- Aspirin Induced Glioma Apoptosis through Noxa Upregulation.International journal of molecular sciences · 2020Article
- Article
Corrections and comments
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Authors and funding
8 authors at 7 institutions in 1 country.
Funding
Abstract
The dormancy of cellular apoptotic machinery has been highlighted as a crucial factor in therapeutic resistance, recurrence, and poor prognosis in patients with malignancy, such as malignant glioma. Increasing evidence indicates that nonsteroidal anti-inflammatory drugs (NSAIDs) confer chemopreventive effects, and indomethacin has been shown to have a novel chemotherapeutic application targeting glioma cells. To extend these findings, herein, we studied the underlying mechanisms of apoptosis activation caused by indomethacin in human H4 and U87 glioma cells. We found that the glioma cell-killing effects of indomethacin involved both death receptor- and mitochondria-mediated apoptotic cascades. Indomethacin-induced glioma cell apoptosis was accompanied by a series of biochemical changes, including reactive oxygen species generation, endoplasmic reticulum (ER) stress, apoptosis signal-regulating kinase-1 (Ask1) activation, p38 hyperphosphorylation, protein phosphatase 2A (PP2A) activation, Akt dephosphorylation, Mcl-1 and FLICE-inhibiting protein (FLIP) downregulation, Bax mitochondrial distribution, and caspases 3/caspase 8/caspase 9 activation. Data on pharmacological inhibition related to oxidative stress, ER stress, free Ca
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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.