Evidence map›Paper›PMID 25112874›Full record

ArticleThe Journal of biological chemistry2014

Chemotherapeutic drugs induce ATP release via caspase-gated pannexin-1 channels and a caspase/pannexin-1-independent mechanism.

Andrea Boyd-Tressler, Silvia Penuela, Dale W Laird, George R Dubyak

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

45 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
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  7. Review
  8. Pannexin1 channels in the liver: an open enemy.Frontiers in cell and developmental biology · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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  17. Article
  18. Targeting CD39 in cancer.Nature reviews. Immunology · 2020
    Review
  19. Article
  20. [Down-regulation of pannexin 2 channel enhances cisplatin-induced apoptosis in testicular cancer I-10 cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020
    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.

Andrea Boyd-TresslerDepartments of Pharmacology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106.
Silvia PenuelaDepartment of Anatomy and Cell Biology, University of Western Ontario, London, Ontario N6A-SC1, Canada.
Dale W LairdDepartment of Anatomy and Cell Biology, University of Western Ontario, London, Ontario N6A-SC1, Canada.
George R DubyakDepartments of Pharmacology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106; Departments of Physiology and Biophysics and Case Western Reserve University School of Medicine, Cleveland, Ohio 44106; Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106 and. Electronic address: george.dubyak@case.edu.
University School · USWestern University · CA

Funding

TRANSMEMBRANE SIGNALLING IN SMOOTH MUSCLE CELL LINESR01GM036387 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI DUBYAK, GEORGE R · 1987 to 2014
$4.5M
PREDOCTORAL TRAINING PROGRAM IN MOLECULAR THERAPEUTICST32GM008803 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI MIEYAL, JOHN J, NIEMAN, MARVIN THOMAS · 2001 to 2023
$4.2M
CIHR MOP130530NIGMS NIH HHS R01 GM036387NIGMS NIH HHS R01-GM36387NIGMS NIH HHS T32-GM008803
6 · The paper itself

Abstract

Anti-tumor immune responses have been linked to the regulated release of ATP from apoptotic cancer cells to engage P2 purinergic receptor signaling cascades in nearby leukocytes. We used the Jurkat T cell acute lymphocytic leukemia model to characterize the role of pannexin-1 (Panx1) channels in the release of nucleotides during chemotherapeutic drug-induced apoptosis. Diverse pro-apoptotic drugs, including topoisomerase II inhibitors, kinase inhibitors, and proteosome inhibitors, induced functional activation of Panx1 channels via caspase-3-mediated cleavage of the Panx1 autoinhibitory C-terminal domain. The caspase-activated Panx1 channels mediated efflux of ATP, but also ADP and AMP, with the latter two comprising >90% of the released adenine nucleotide pool as cells transitioned from the early to late stages of apoptosis. Chemotherapeutic drugs also activated an alternative caspase- and Panx1-independent pathway for ATP release from Jurkat cells in the presence of benzyloxycarbonyl-VAD, a pan-caspase inhibitor. Comparison of Panx1 levels indicated much higher expression in leukemic T lymphocytes than in normal, untransformed T lymphoblasts. This suggests that signaling roles for Panx1 may be amplified in leukemic leukocytes. Together, these results identify chemotherapy-activated pannexin-1 channels and ATP release as possible mediators of paracrine interaction between dying tumor cells and the effector leukocytes that mediate immunogenic anti-tumor responses.

Indexed as

Adenosine DiphosphateAdenosine TriphosphateAntineoplastic AgentsApoptosisCaspase 3Caspase InhibitorsConnexinsHumansJurkat CellsNeoplasm ProteinsNerve Tissue ProteinsPrecursor Cell Lymphoblastic Leukemia-LymphomaAdenosine DiphosphateAdenosine TriphosphateAntineoplastic AgentsCASP3 protein, humanCaspase 3Caspase InhibitorsConnexinsNeoplasm ProteinsNerve Tissue ProteinsPANX1 protein, humanApoptosisATPCaspasePannexinPurinergic Agonist

Identifiers

PMID25112874
PMCPMC4175357
OpenAlexW2050688486

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.