ReviewMedComm2025
Endoplasmic Reticulum Stress in Cancer.
Review in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed.
- Advances in SEC61G research: from ER translocon subunit to emerging pan-cancer oncogenic roles.Cancer biology & therapy · 2026Review
- Multi-omics and machine learning identify ALOX5 as a ferroptosis-associated driver of epithelial barrier dysfunction in chronic rhinosinusitis with nasal polyps.The World Allergy Organization journal · 2026Article
- Chrysosplenetin-induced TMED3 aggregation triggers unfolded protein response in pancreatic cancer.EMBO molecular medicine · 2026Article
- GRP78 Drives NSCLC Stemness and EMT via a SIX1/β-Catenin Signaling Axis.Drug development research · 2026Article
- Spiramide and Hydroquinidine Inhibit Proliferation and Migration While Promoting Apoptosis and Oxidative Stress in Neuroblastoma Cells.International journal of molecular sciences · 2026Article
- Prognostic RNA-splicing archetypes in breast cancer identified by extended pre-training of histopathology foundation models.Nature communications · 2026Article
- Multifunctional nanotherapeutics for targeted modulation of endoplasmic reticulum stress to potentiate cancer therapy.Asian journal of pharmaceutical sciences · 2026Review
- Endoplasmic Reticulum-Targeting NIR Cyanine ER800 Nanoparticles Promote Pyroptosis in Triple-Negative Breast Cancer.ACS applied materials & interfaces · 2026Article
- Overcoming ADC resistance in advanced colorectal cancer by dual targeting of TROP2 and PERK to suppress Wnt/β-catenin signaling.Cell reports. Medicine · 2026Article
- PABPC1-induced stabilization of PGK1 mRNA reduces apoptosis and sunitinib sensitivity in renal cell carcinoma by suppressing endoplasmic reticulum stress.Cell death & disease · 2026Article
- Pyra-metho-carnil disrupts cancer cell proteostasis and induces apoptosis by binding to KDEL receptors.Scientific reports · 2026Article
- Targeting LIPA with ERX-41 Induces ER Stress and Inhibits Tumor Progression in Inflammatory Breast Cancer.Biomolecules · 2026Article
- The Interplay Between CaCells · 2026Review
- Unveiling ER-Phagy Receptors in Thyroid Cancer: A Combined Approach of Public Data Mining and In Vitro Validation.Clinical Medicine Insights. Oncology · 2026Article
- TRAIL of Hope: Bioactive Dietary Component-Driven Carrier-Free Nanoplatforms for Synergistically Enhanced Tumor Multimodal Therapy.International journal of nanomedicine · 2026Review
- LRRC59 inhibits perk pathway‑induced apoptosis and promotes cell proliferation, migration and invasion in colorectal cancer cells.Oncology reports · 2026Article
- Targeting the unfolded protein response in cancer: mechanisms, small-molecule inhibitors, and translational challenges.Frontiers in immunology · 2026Review
- GDF15-integrated blood biomarker panel for risk stratification of digestive malignancies: a multicenter retrospective study.Frontiers in pharmacology · 2026Article
- Gut microbiota-derived metabolites in immunomodulation and gastrointestinal cancer immunotherapy.Frontiers in immunology · 2025Review
- The Role of UFMylation in the Development and Progression of Gastric Cancer.Oncology research · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Persistent and intense endoplasmic reticulum (ER) stress is widely acknowledged as a hallmark of tumorigenesis. To restore ER homeostasis, cells activate the unfolded protein response (UPR), which is aberrantly regulated in cancer cells. This review provides an in-depth analysis of the mechanisms through which the UPR facilitates tumor progression. The UPR is activated by ER stress sensors such as inositol-requiring enzyme 1 (IRE1α), protein kinase R-like ER-resident kinase (PERK), and activating transcription factor 6 (ATF6). These sensors regulate cancer cell proliferation, immune evasion, metastasis, and drug resistance. We summarize the crosstalk between the UPR and multiple signaling pathways, including mTOR, MAPK, and NF-κB, which collectively promote tumor growth and metastasis. Additionally, we discuss the role of the UPR in modulating the tumor microenvironment to support angiogenesis and immune evasion. We also provide an overview of pharmacological agents targeting specific UPR pathways, such as GRP78 inhibitors, IRE1α inhibitors, PERK inhibitors, and ATF6 inhibitors, with the aim of developing more effective cancer therapies. This comprehensive review highlights the potential of targeting the UPR as a novel strategy for cancer treatment and underscores the need for further research to elucidate the complex interactions between the UPR and cancer progression.
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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.