ArticleNature communications2021
Apoptotic stress-induced FGF signalling promotes non-cell autonomous resistance to cell death.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 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
28 citing papers in PubMed, 42 citations in OpenAlex.
- PPARβ/δ priming enhances mesenchymal stromal cell anti-apoptotic properties on chondrocytes via ANGPTL4 and improves their therapeutic effects in osteoarthritis.Stem cells translational medicine · 2026Article
- The signaling and regulatory functions of dying cells and cell corpses.Communications biology · 2026Review
- Mutated FGFR1 is an oncogenic driver and therapeutic target in high-risk neuroblastoma.The Journal of clinical investigation · 2026Article
- Dying cells as architects of the stem cell niche: a conserved mechanism driving tissue regeneration and tumor therapy resistance.Cell communication and signaling : CCS · 2026Review
- Atypical contribution of caspase-3 to melanoma cancer cell motility by regulation of coronin 1B activity.Cell death & disease · 2025Article
- Angiogenesis, signaling pathways, and animal models.Chinese medical journal · 2025Review
- Gastrointestinal acute radiation syndrome: current knowledge and perspectives.Cell death discovery · 2025Review
- Of Tingible Bodies and Starry Skies: Control of Normal and Malignant Tissues Through Apoptotic Cell-Dependent Communication (ACDC).Advances in experimental medicine and biology · 2025Review
- Article
- Reduction of endocytosis and EGFR signaling is associated with the switch from isolated to clustered apoptosis during epithelial tissue remodeling in Drosophila.PLoS biology · 2024Article
- Stress in the metastatic journey - the role of cell communication and clustering in breast cancer progression and treatment resistance.Disease models & mechanisms · 2024Article
- Morphologically transformable peptide nanocarriers coloaded with doxorubicin and curcumin inhibit the growth and metastasis of hepatocellular carcinoma.Materials today. Bio · 2024Article
- Hijacking homeostasis: Regulation of the tumor microenvironment by apoptosis.Immunological reviews · 2023Review
- Review
- Extracellular vesicles arising from apoptosis: forms, functions, and applications.The Journal of pathology · 2023Review
- DeXtrusion: automatic recognition of epithelial cell extrusion through machine learning in vivo.Development (Cambridge, England) · 2023Article
- Non-lethal outcomes of engaging regulated cell death pathways in cancer.Nature cancer · 2023Review
- Cell death, therapeutics, and the immune response in cancer.Trends in cancer · 2023Review
- Preparation strategy of hydrogel microsphere and its application in skin repair.Frontiers in bioengineering and biotechnology · 2023Review
- LncRNAs and regulated cell death in tumor cells.Frontiers in oncology · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
Abstract
Damaged or superfluous cells are typically eliminated by apoptosis. Although apoptosis is a cell-autonomous process, apoptotic cells communicate with their environment in different ways. Here we describe a mechanism whereby cells under apoptotic stress can promote survival of neighbouring cells. We find that upon apoptotic stress, cells release the growth factor FGF2, leading to MEK-ERK-dependent transcriptional upregulation of pro-survival BCL-2 proteins in a non-cell autonomous manner. This transient upregulation of pro-survival BCL-2 proteins protects neighbouring cells from apoptosis. Accordingly, we find in certain cancer types a correlation between FGF-signalling, BCL-2 expression and worse prognosis. In vivo, upregulation of MCL-1 occurs in an FGF-dependent manner during skin repair, which regulates healing dynamics. Importantly, either co-treatment with FGF-receptor inhibitors or removal of apoptotic stress restores apoptotic sensitivity to cytotoxic therapy and delays wound healing. These data reveal a pathway by which cells under apoptotic stress can increase resistance to cell death in surrounding cells. Beyond mediating cytotoxic drug resistance, this process also provides a potential link between tissue damage and repair.
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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.