ArticleProceedings of the National Academy of Sciences of the United States of America2023
Cell survival following direct executioner-caspase activation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. 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 31 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.
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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.
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- Anastasis: an unwelcome guest in cancer therapy.Apoptosis : an international journal on programmed cell death · 2026Review
- Tumor gasdermin E acts as a rheostat to limit apoptotic cell survival and mutagenesis in anticancer immune environments.Science advances · 2026Article
- Resurrection biology: Melatonin as a modulator of anastasis (Review).Molecular medicine reports · 2026Review
- Evasion of cell death despite mitochondrial outer membrane permeabilization: an oncogenic outcome of apoptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Caspase-1 inhibition: mechanistic insights and comprehensive review of reported inhibitors to date.Inflammopharmacology · 2026Review
- Regulated cell death plasticity in cancer: thresholds, reversibility, and therapeutic failure.Journal of translational medicine · 2026Review
- Therapeutic potential of BH3-mimetics and NK cell-mediated immunotherapy in T-ALL.Cell death & disease · 2026Article
- Article
- A kinome inhibitor screen implicates adhesion and growth factor signaling in cellular recovery after caspase activation.bioRxiv : the preprint server for biology · 2026Article
- DNA fragmentation factor B suppresses interferon to enable cancer persister cell regrowth.Nature cell biology · 2025Article
- Drug-tolerant persister cells in cancer: bridging the gaps between bench and bedside.Nature communications · 2025Review
- Back from the brink: programmed cell revival for regeneration.The EMBO journal · 2025Article
- Programmed cell revival from imminent cell death enhances tissue repair and regeneration.The EMBO journal · 2025Article
- Unravelling the pathological roles of anastasis in cancer recurrence.Open biology · 2025Review
- Apoptotic Caspases-3 and -7 Cleave Extracellular Domains of Membrane-Bound Proteins from MDA-MB-231 Breast Cancer Cells.International journal of molecular sciences · 2025Article
- Applying Ultrasound to Mechanically and Noninvasively Sensitize Prostate Tumors to TRAIL-Mediated Apoptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Using a Natural Triterpenoid to Unlock the Antitumor Effects of Autophagy in B-Cell Lymphoma.Biomedicines · 2025Article
- The EMCV protein 2B* is required for efficient cell lysis via both caspase-3-dependent and -independent pathways during infection.The Journal of general virology · 2025Article
- Insights into the Mode of Action of Novel Morpholinated Curcumin Derivatives Exhibiting Potent Antitumor Activity in Bladder Cancer Cells In Vitro.Molecules (Basel, Switzerland) · 2025Article
- Targeted Activation of Programmed Cell Death Pathways by Optogenetics.Methods in molecular biology (Clifton, N.J.) · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Executioner-caspase activation has been considered a point-of-no-return in apoptosis. However, numerous studies report survival from caspase activation after treatment with drugs or radiation. An open question is whether cells can recover from direct caspase activation without pro-survival stress responses induced by drugs. To address this question, we engineered a HeLa cell line to express caspase-3 inducibly and combined it with a quantitative caspase activity reporter. While high caspase activity levels killed all cells and very low levels allowed all cells to live, doses of caspase activity sufficient to kill 15 to 30% of cells nevertheless allowed 70 to 85% to survive. At these doses, neither the rate, nor the peak level, nor the total amount of caspase activity could accurately predict cell death versus survival. Thus, cells can survive direct executioner-caspase activation, and variations in cellular state modify the outcome of potentially lethal caspase activity. Such heterogeneities may underlie incomplete tumor cell killing in response to apoptosis-inducing cancer treatments.
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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.