Evidence map›Paper›PMID 35443185›Full record

ArticleCell reports2022

Non-apoptotic activation of Drosophila caspase-2/9 modulates JNK signaling, the tumor microenvironment, and growth of wound-like tumors.

Derek Cui Xu, Li Wang, Kenneth M Yamada, Luis Alberto Baena-Lopez

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Macrophage restriction inScience advances · 2026
    Article
  2. Review
  3. Caspase-1 in cancer and inflammatory diseases: a potential therapeutic target.Apoptosis : an international journal on programmed cell death · 2026
    Review
  4. Article
  5. Article
  6. The Power of Drosophila in Modeling Cancer Cachexia.Advances in experimental medicine and biology · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Apoptosis inhibition restrains primary malignant traits in differentFrontiers in cell and developmental biology · 2022
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Derek Cui XuCell Biology Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4370, USA; Sir William Dunn School of Pathology, University of Oxford, Oxford, Oxfordshire OX1 3RE, UK.
Li WangSir William Dunn School of Pathology, University of Oxford, Oxford, Oxfordshire OX1 3RE, UK.
Kenneth M YamadaCell Biology Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4370, USA. Electronic address: kenneth.yamada@nih.gov.
Luis Alberto Baena-LopezSir William Dunn School of Pathology, University of Oxford, Oxford, Oxfordshire OX1 3RE, UK. Electronic address: alberto.baenalopez@path.ox.ac.uk.
National Institutes of Health · USUniversity of Oxford · GB

Funding

Cell-Surface Interactions in PathogenesisZIADE000719 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI YAMADA, KENNETH · 2009 to 2025
$13.5M
Cell-Matrix Interactions and MigrationZIADE000524 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI YAMADA, KENNETH · 2009 to 2025
$10.2M
Cell-Surface Interactions in PathogenesisZ01DE000719 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI YAMADA, KENNETH · 2007 to 2008
$824k
Cancer Research UK 17516Cancer Research UK C49979/A17516Intramural NIH HHS Z01 DE000719Intramural NIH HHS ZIA DE000719
6 · The paper itself

Abstract

Resistance to apoptosis due to caspase deregulation is considered one of the main hallmarks of cancer. However, the discovery of novel non-apoptotic caspase functions has revealed unknown intricacies about the interplay between these enzymes and tumor progression. To investigate this biological problem, we capitalized on a Drosophila tumor model with human relevance based on the simultaneous overactivation of the EGFR and the JAK/STAT signaling pathways. Our data indicate that widespread non-apoptotic activation of initiator caspases limits JNK signaling and facilitates cell fate commitment in these tumors, thus preventing the overgrowth and exacerbation of malignant features of transformed cells. Intriguingly, caspase activity also reduces the presence of macrophage-like cells with tumor-promoting properties in the tumor microenvironment. These findings assign tumor-suppressing activities to caspases independent of apoptosis, while providing molecular details to better understand the contribution of these enzymes to tumor progression.

Indexed as

Drosophila ProteinsNeoplasmsAnimalsApoptosisCaspase 2CaspasesDrosophilaDrosophila melanogasterTumor MicroenvironmentCaspase 2CaspasesDrosophila ProteinsCaspase-9CP: Cell biologyDroncDrosophila wound-like tumorEGFR signalinghemocytesJAK/STAT signalingJNK signalingnon-apoptotic caspase activationtumor-associated macrophagestumor suppressor

Identifiers

PMID35443185
PMCPMC9082238
OpenAlexW4224246332

What Socratic holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.