ReviewInternational journal of molecular sciences2023
Endoplasmic Reticulum Stress in Renal Cell Carcinoma.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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
17 citing papers in PubMed, 23 citations in OpenAlex.
- Unfolded Protein Response Pathways in Cancer: Mechanisms, Tumor Biology and Therapeutic Opportunities.Molecular diagnosis & therapy · 2026Review
- PABPC1-induced stabilization of PGK1 mRNA reduces apoptosis and sunitinib sensitivity in renal cell carcinoma by suppressing endoplasmic reticulum stress.Cell death & disease · 2026Article
- Multifaceted role of CNPY2 beyond ER stress: Disease implications and therapeutic potential.Cell stress · 2026Article
- Prognostic role of eIF2α protein in metastatic renal cell cancer patients.Discover oncology · 2025Article
- Identification and Verification of Endoplasmic Reticulum Stress-Related Genes as Novel Signatures for Osteoarthritis Diagnosis and Therapy: A Bioinformatics Analysis-Oriented Pilot Study.Biochemical genetics · 2025Article
- Endoplasmic Reticulum Stress in Tuberculosis: Molecular Bases and Pathophysiological Implications in the Immunopathogenesis of the Disease.International journal of molecular sciences · 2025Review
- Targeting polyunsaturated fatty acids desaturase FADS1 inhibits renal cancer growth via ATF3-mediated ER stress response.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- 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
- Article
- Network pharmacology and in silico analysis ofIn silico pharmacology · 2025Article
- Nanotechnology-Based Strategies for Safe and Effective Immunotherapy.Molecules (Basel, Switzerland) · 2024Review
- The Cellular Stress and Cutaneous Manifestations in Renal Cell Carcinomas-A Narrative Review.Journal of clinical medicine · 2024Review
- Identifying endoplasmic reticulum stress-related genes as new diagnostic and prognostic biomarkers in clear cell renal cell carcinoma.Translational andrology and urology · 2024Article
- Article
- Redox Signaling Modulates Activity of Immune Checkpoint Inhibitors in Cancer Patients.Biomedicines · 2023Review
- Crosstalk between endoplasmic reticulum stress and multidrug-resistant cancers: hope or frustration.Frontiers in pharmacology · 2023Review
- Construction and validation of predictive model based on endoplasmic reticulum stress-related genes for triple-negative breast cancer.Cell cycle (Georgetown, Tex.)Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The endoplasmic reticulum is an organelle exerting crucial functions in protein production, metabolism homeostasis and cell signaling. Endoplasmic reticulum stress occurs when cells are damaged and the capacity of this organelle to perform its normal functions is reduced. Subsequently, specific signaling cascades, together forming the so-called unfolded protein response, are activated and deeply impact cell fate. In normal renal cells, these molecular pathways strive to either resolve cell injury or activate cell death, depending on the extent of cell damage. Therefore, the activation of the endoplasmic reticulum stress pathway was suggested as an interesting therapeutic strategy for pathologies such as cancer. However, renal cancer cells are known to hijack these stress mechanisms and exploit them to their advantage in order to promote their survival through rewiring of their metabolism, activation of oxidative stress responses, autophagy, inhibition of apoptosis and senescence. Recent data strongly suggest that a certain threshold of endoplasmic reticulum stress activation needs to be attained in cancer cells in order to shift endoplasmic reticulum stress responses from a pro-survival to a pro-apoptotic outcome. Several endoplasmic reticulum stress pharmacological modulators of interest for therapeutic purposes are already available, but only a handful were tested in the case of renal carcinoma, and their effects in an in vivo setting remain poorly known. This review discusses the relevance of endoplasmic reticulum stress activation or suppression in renal cancer cell progression and the therapeutic potential of targeting this cellular process for this cancer.
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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.