ReviewOncogene2016
The evolving paradigm of cell-nonautonomous UPR-based regulation of immunity by cancer cells.
Review in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 48 citations in OpenAlex.
- Cancer pain: molecular mechanisms and management.Molecular biomedicine · 2025Review
- Article
- Delivery of miR-214 via extracellular vesicles downregulatesExtracellular vesicles and circulating nucleic acids · 2024Article
- Endoplasmic reticular stress as an emerging therapeutic target for chronic pain: a narrative review.British journal of anaesthesia · 2024Review
- Endoplasmic Reticulum Stress in the Brain Tumor Immune Microenvironment.Molecular cancer research : MCR · 2023Article
- The impact of TP53 activation and apoptosis in primary hereditary microcephaly.Frontiers in neuroscience · 2023Review
- A systemic cell stress signal confers neuronal resilience toward oxidative stress in a Hedgehog-dependent manner.Cell reports · 2022Article
- Mitochondrial fission induces immunoescape in solid tumors through decreasing MHC-I surface expression.Nature communications · 2022Article
- High Expression of CKS2 Predicts Adverse Outcomes: A Potential Therapeutic Target for Glioma.Frontiers in immunology · 2022Article
- The Unfolded Protein Response at the Tumor-Immune Interface.Frontiers in immunology · 2022Review
- Karyotype Aberrations in Action: The Evolution of Cancer Genomes and the Tumor Microenvironment.Genes · 2021Review
- Endoplasmic Reticulum Homeostasis and Stress Responses in Caenorhabditis elegans.Progress in molecular and subcellular biology · 2021Article
- The UPR in Neurodegenerative Disease: Not Just an Inside Job.Biomolecules · 2020Review
- IRE1α and IGF signaling predict resistance to an endoplasmic reticulum stress-inducing drug in glioblastoma cells.Scientific reports · 2020Observational
- No evidence for cell-to-cell transmission of the unfolded protein response in cell culture.Journal of neurochemistry · 2020Article
- Transmissible Endoplasmic Reticulum Stress: A Novel Perspective on Tumor Immunity.Frontiers in cell and developmental biology · 2020Review
- Hypoxia induces immunogenic cell death of cancer cells by enhancing the exposure of cell surface calreticulin in an endoplasmic reticulum stress-dependent manner.Oncology letters · 2019Article
- Endoplasmic reticulum stress is transmissible in vitro between cells of the central nervous system.Journal of neurochemistry · 2019Article
- Polyphenol-rich extract induces apoptosis with immunogenic markers in melanoma cells through the ER stress-associated kinase PERK.Cell death discovery · 2019Article
- Mechanisms regulating immune surveillance of cellular stress in cancer.Cellular and molecular life sciences : CMLS · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The endoplasmic reticulum (ER) stress response/unfolded protein response (UPR) has been thought to influence tumorigenesis mainly through cell-intrinsic, pro-survival effects. In recent years, however, new evidence has emerged showing that the UPR is also the source of cell-extrinsic effects, particularly directed at those immune cells within the tumor microenvironment. Here we will review and discuss this new body of information with focus on the role of cell-extrinsic effects on innate and adaptive immunity, suggesting that the transmission of ER stress from cancer cells to myeloid cells in particular is an expedient used by cancer cells to control the immune microenvironment, which acquires pro-inflammatory as well as immune-suppressive characteristics. These new findings can now be seen in the broader context of similar phenomena described in Caenorhabditis elegans, and an analogy with quorum sensing and 'community effects' in prokaryotes and eukaryotes can be drawn, arguing that a cell-nonautonomous UPR-based regulation of heterologous cells may be phylogenetically conserved. Finally, we will discuss the role of aneuploidy as an inducer of proteotoxic stress and potential initiator of cell-nonautonomous UPR-based regulation. In presenting these new views, we wish to bring attention to the cell-extrinsic regulation of tumor growth, including tumor UPR-based cell-nonautonomous signaling as a mechanism of maintaining tumor heterogeneity and resistance to therapy, and suggest therapeutically targeting such mechanisms within the tumor microenvironment.
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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.