ArticleBritish journal of cancer2018
Increased sensitivity to apoptosis upon endoplasmic reticulum stress-induced activation of the unfolded protein response in chemotherapy-resistant malignant pleural mesothelioma.
Article in British journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- De novo pyrimidine synthesis is a collateral metabolic vulnerability in NF2-deficient mesothelioma.EMBO molecular medicine · 2025Article
- An Overview of Cellular and Molecular Determinants Regulating Chemoresistance in Pleural Mesothelioma.Cancers · 2025Review
- Leveraging Immunogenic Cell Death to Enhance the Immune Response against Malignant Pleural Mesothelioma Tumors.Journal of the American Chemical Society · 2025Article
- Modulating the unfolded protein response with ISRIB mitigates cisplatin ototoxicity.Scientific reports · 2024Article
- Endoplasmic reticulum stress and quality control in relation to cisplatin resistance in tumor cells.Frontiers in pharmacology · 2024Review
- Dissecting the Immunological Profiles inCancers · 2022Article
- Schedule-Dependent Treatment Increases Chemotherapy Efficacy in Malignant Pleural Mesothelioma.International journal of molecular sciences · 2022Article
- Organoids as a Model for Precision Medicine in Malignant Pleural Mesothelioma: Where Are We Today?Cancers · 2022Review
- Metabolic synthetic lethality by targeting NOP56 and mTOR in KRAS-mutant lung cancer.Journal of experimental & clinical cancer research : CR · 2022Article
- Mitochondria inter-organelle relationships in cancer protein aggregation.Frontiers in cell and developmental biology · 2022Review
- Review
- Chemotherapy-induced CDA expression renders resistant non-small cell lung cancer cells sensitive to 5'-deoxy-5-fluorocytidine (5'-DFCR).Journal of experimental & clinical cancer research : CR · 2021Article
- Malignant pleural mesothelioma co-opts BCL-XCell death & disease · 2021Article
- Targeting histone deacetylase enhances the therapeutic effect of Erastin-induced ferroptosis inTranslational lung cancer research · 2021Article
- Pharmacotranscriptomic Analysis Reveals Novel Drugs and Gene Networks Regulating Ferroptosis in Cancer.Cancers · 2020Article
- Inducing endoplasmic reticulum stress in cancer cells using graphene oxide-based nanoparticles.Nanoscale advances · 2020Article
- The integrated stress response in pulmonary disease.European respiratory review : an official journal of the European Respiratory Society · 2020Review
- Proteotoxic Stress and Cell Death in Cancer Cells.Cancers · 2020Review
- Exploring the In Vivo and In Vitro Anticancer Activity of Rhenium Isonitrile Complexes.Inorganic chemistry · 2020Article
- Biomarker-guided targeted and immunotherapies in malignant pleural mesothelioma.Therapeutic advances in medical oncology · 2020Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundStandard treatment for advanced malignant pleural mesothelioma (MPM) is a cisplatin/pemetrexed (MTA) regimen; however, this is confronted by drug resistance. Proteotoxic stress in the endoplasmic reticulum (ER) is a hallmark of cancer and some rely on this stress signalling in response to cytotoxic chemotherapeutics. We hypothesise that ER stress and the adaptive unfolded protein response (UPR) play a role in chemotherapy resistance of MPM.
methodsIn vitro three-dimensional (3D) and ex vivo organotypic culture were used to enrich a chemotherapy-resistant population and recapitulate an in vivo MPM microenvironment, respectively. Markers of ER stress, the UPR and apoptosis were assessed at mRNA and protein levels. Cell viability was determined based on acid phosphatase activity.
resultsMPM cells with de novo and/or acquired chemotherapy resistance displayed low ER stress, which rendered the cells hypersensitive to agents that induce ER stress and alter the UPR. Bortezomib, an FDA-approved proteasome inhibitor, selectively impairs chemotherapy-resistant MPM cells by activating the PERK/eIF2α/ATF4-mediated UPR and augmenting apoptosis.
conclusionsWe provide the first evidence for ER stress and the adaptive UPR signalling in chemotherapy resistance of MPM, which suggests that perturbation of the UPR by altering ER stress is a novel strategy to treat chemotherapy-refractory MPM.
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