ReviewFrontiers in oncology2017
Endoplasmic Reticulum Stress, Unfolded Protein Response, and Cancer Cell Fate.
Review in Frontiers in oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 211 papers.
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Who cites it
211 citing papers in PubMed.
- BRAP maintains SEC24D stability to regulate ER stress and promote cervical adenocarcinoma progression.Journal of translational medicine · 2026Article
- On the Edge of Benefit and Harm: Reactive Oxygen Species in Cancer.International journal of molecular sciences · 2026Review
- Enterococcus faecalis and lipoteichoic acid up-regulated PD-L1 of macrophage through TLR and IRE1 α/XBP1 signaling axis.Odontology · 2026Article
- The influence of exercise duration on inhibiting endoplasmic reticulum stress in ischemic stroke rats.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Article
- Mitotic catastrophe-related six-gene signature predicts prognosis, tumor immune landscape, and therapeutic response in lung adenocarcinoma.BMC medical genomics · 2026Article
- Autophagy-Apoptosis Crosstalk in Cancer: Mechanisms, Signaling Pathways, and Therapeutic Targeting.Cancers · 2026Review
- Targeting endoplasmic reticulum stress for neuroprotection in ischemia-reperfusion injury: mechanisms and therapeutic approaches.Molecular biology reports · 2026Review
- UC2288 decreases the viability and metastatic activity of human Uveal melanoma cells via activating the AMPK/eIF2/ATF4 ER stress axis.European journal of pharmacology · 2026Article
- Mitochondrial Calcium Signaling in Hepatocyte Health and Disease.Cold Spring Harbor perspectives in biology · 2026Review
- Functional interplay between endoplasmic reticulum stress and mitochondrial activity in a post-ovulatory aging model of mouse oocytes.Journal of assisted reproduction and genetics · 2026Article
- Necrotic Cells Alter IRE1α-XBP1 Signaling and Induce Transcriptional Changes in Glioblastoma.International journal of molecular sciences · 2026Article
- DCAF12 Ubiquitin Ligase Promotes Lung Cancer Metastasis by Modulating the TRiC/CCT Chaperonin Complex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Autocrine and paracrine regulation of pituitary endocrine cells.Frontiers in endocrinology · 2026Review
- Navigating Cellular Stress: Endoplasmic Reticulum Stress and the Unfolded Protein Response in the Molecular Pathogenesis of Preeclampsia.Cell biochemistry and biophysics · 2025Review
- Pinpointing an innovative autophagic signature as a prognostic and diagnostic biomarkers in colorectal carcinoma.Future science OA · 2025Article
- Senkyunolide A ameliorates cholestatic liver fibrosis by controlling CLCC1-mediated endoplasmic reticulum CaActa pharmacologica Sinica · 2025Article
- The Unfolded Protein Response-Novel Mechanisms, Challenges, and Key Considerations for Therapeutic Intervention.Cancers · 2025Review
- Lipid metabolism orchestrates liver regeneration: an integrated metabolic network.Journal of translational medicine · 2025Review
- COPB2 facilitates EDEM3-mediated mannose trimming to sustain ER homeostasis in ovarian cancer.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Investigating the molecular mechanisms of phytochemicals targeting Ras-related C3 botulinum toxin substrate 1 (Rac1) to inhibit breast cancer metastasis via endoplasmic reticulum stress and Wnt-PCP signaling pathway.Journal of molecular modeling · 2025Article
151 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Perturbation of endoplasmic reticulum (ER) homeostasis results in a stress condition termed "ER stress" determining the activation of a finely regulated program defined as unfolded protein response (UPR) and whose primary aim is to restore this organelle's physiological activity. Several physiological and pathological stimuli deregulate normal ER activity causing UPR activation, such as hypoxia, glucose shortage, genome instability, and cytotoxic compounds administration. Some of these stimuli are frequently observed during uncontrolled proliferation of transformed cells, resulting in tumor core formation and stage progression. Therefore, it is not surprising that ER stress is usually induced during solid tumor development and stage progression, becoming an hallmark of such malignancies. Several UPR components are in fact deregulated in different tumor types, and accumulating data indicate their active involvement in tumor development/progression. However, although the UPR program is primarily a pro-survival process, sustained and/or prolonged stress may result in cell death induction. Therefore, understanding the mechanism(s) regulating the cell survival/death decision under ER stress condition may be crucial in order to specifically target tumor cells and possibly circumvent or overcome tumor resistance to therapies. In this review, we discuss the role played by the UPR program in tumor initiation, progression and resistance to therapy, highlighting the recent advances that have improved our understanding of the molecular mechanisms that regulate the survival/death switch.
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