ReviewCancer genomics & proteomics
The Role of ER Stress and the Unfolded Protein Response in Cancer.
Review in Cancer genomics & proteomics. 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
- Discovery of PIM-1 kinase inhibitors from marine natural products through machine learning and structure-based screening.Research in pharmaceutical sciences · 2026Article
- Inhibiting endoplasmic reticulum stress and unfolded protein response: an effective strategy for chemoprevention of hepatocarcinogenesis.Molecular and cellular biochemistry · 2026Article
- Article
- Article
- Muscle invasion in bladder cancer is associated with increased expression of ATG5, LC3A and CHOP.Molecular biology reports · 2026Article
- Differential Effects of PERK and IRE1α Silencing on Expression of Apoptosis and Autophagy Markers in T-Lymphoblastic Leukemia MOLT-3 Cells.International journal of molecular sciences · 2026Article
- Inhibition of SIK2 and SIK3 induces adaptive ER-phagy and creates a therapeutic vulnerability in ovarian cancer.Research square · 2026Article
- Autophagy-Apoptosis Crosstalk in Cancer: Mechanisms, Signaling Pathways, and Therapeutic Targeting.Cancers · 2026Review
- Metformin triggers apoptosis via endoplasmic reticulum stress in HER2-positive breast cancer cell lines.Experimental and therapeutic medicine · 2026Article
- The role of glycoproteins in autophagy and apoptosis in colorectal cancer: A scoping review.Medical oncology (Northwood, London, England) · 2026Article
- Mapping metabolic reprogramming in lung and breast cancer through integrative bioinformatics.PloS one · 2026Article
- Article
- Engineering endoplasmic reticulum targeted metal-polyphenol curcumin nanomicelles for melanoma therapy.Journal of nanobiotechnology · 2025Article
- Targeting Cancer Through Thymoquinone: From Molecular Mechanisms to Clinical Prospects.International journal of molecular sciences · 2025Review
- The Role of Endoplasmic Reticulum Stress and Unfolded Protein Response in Gynecological Cancers: A Narrative Review.Cureus · 2025Review
- Modulation of Endoplasmic Reticulum Stress in Experimental Anti-Cancer Therapy.International journal of molecular sciences · 2025Review
- Endoplasmic reticulum stress in non-small cell lung cancer: a review of therapeutic agents, mechanistic insights, and implications for therapy.Frontiers in cell and developmental biology · 2025Review
- Rutin Suppresses EMT and Induces Mitochondrial BiogenesisCancer genomics & proteomicsArticle
- Immunohistochemical Analysis of IRE1 and PERK Expression in Extravillous Trophoblast Cells of Placenta Accreta Spectrum and Associations With Clinicopathological Parameters.In vivo (Athens, Greece)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulation of protein synthesis, folding, and secretion leads to endoplasmic reticulum (ER) stress, triggering the unfolded protein response (UPR). While the UPR is essential for cell survival under stress, its chronic activation in cancer cells supports tumorigenesis, metastasis, and chemoresistance by enabling cellular adaptation to hypoxia, nutrient deprivation, and oxidative stress. This review provides a comprehensive overview of the roles of key UPR mediators - binding immunoglobulin protein (BiP), protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK), inositol-requiring enzyme 1α (IRE1α), and activating transcription factor 6 (ATF6) - in cancer progression and therapy resistance. Furthermore, it discusses strategies to target UPR pathways, including small molecule inhibitors, gene therapies, natural compounds, and combination therapies, while it evaluates their preclinical and clinical relevance. Finally, it explores how modulating UPR signaling can overcome therapeutic resistance, improve immunotherapy outcomes, and reshape the tumor microenvironment. This review emphasizes the promise of UPR-targeted approaches in enhancing the efficacy of current cancer treatments and achieving better patient outcomes.
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Identifiers
What OpenQuestion holds
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.