Evidence map›Paper›PMID 27551451›Full record

ArticleCell death discovery2015

Curcumin induces crosstalk between autophagy and apoptosis mediated by calcium release from the endoplasmic reticulum, lysosomal destabilization and mitochondrial events.

A Moustapha, P A Pérétout, N E Rainey, F Sureau, M Geze, J-M Petit, E Dewailly, C Slomianny, P X Petit

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

76 citing papers in PubMed, 151 citations in OpenAlex.

  1. Article
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  5. Curcumin Between Pleiotropic Potential and Translational Constraints.International journal of molecular sciences · 2026
    Review
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  7. Review
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  9. Evaluation of hydrogel loading with curcumin and silver nanoparticles: biocompatibilities and anti-biofilm activities.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025
    Article
  10. Article
  11. Article
  12. Curcumin: a potential anti-photoaging agent.Frontiers in pharmacology · 2025
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article

16 more citing papers are in PubMed but not listed here.

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

9 authors at 4 institutions in 1 country.

A MoustaphaINSERM U1124 'Toxicologie, Pharmacologie et Signalisation Cellulaire', Université Paris-Descartes, Centre Universitaire des Saints-Pères , Paris, France.
P A PérétoutINSERM U1124 'Toxicologie, Pharmacologie et Signalisation Cellulaire', Université Paris-Descartes, Centre Universitaire des Saints-Pères , Paris, France.
N E RaineyINSERM U1124 'Toxicologie, Pharmacologie et Signalisation Cellulaire', Université Paris-Descartes, Centre Universitaire des Saints-Pères , Paris, France.
F SureauUniversité Pierre et Marie Curie-Paris 6, Laboratoire Jean Perrin , Paris, France.
M GezeMuséum National d'Histoire Naturelles, CeMIM/USM 0504, 'Biologie Fonctionnelles des Protozoaires' 57 , Paris, France.
J-M PetitMuséum National d'Histoire Naturelles, UMR 7245 CNRS/MNHN 'Molécules de Communication et Adaptation des Micro-organismes' 57 , Paris, France.
E DewaillyLaboratoire de Physiologie cellulaire, INSERM U800, Université des Sciences et Techniques de Lille 1 , Villeneuve d'Ascq, France.
C SlomiannyLaboratoire de Physiologie cellulaire, INSERM U800, Université des Sciences et Techniques de Lille 1 , Villeneuve d'Ascq, France.
P X PetitINSERM U1124 'Toxicologie, Pharmacologie et Signalisation Cellulaire', Université Paris-Descartes, Centre Universitaire des Saints-Pères , Paris, France.
Inserm · FRUniversité Paris Cité · FRLaboratoire Jean Perrin · FRMolécules de Communication et Adaptation des Micro-organismes · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Curcumin, a major active component of turmeric (Curcuma longa, L.), has anticancer effects. In vitro studies suggest that curcumin inhibits cancer cell growth by activating apoptosis, but the mechanism underlying these effects is still unclear. Here, we investigated the mechanisms leading to apoptosis in curcumin-treated cells. Curcumin induced endoplasmic reticulum stress causing calcium release, with a destabilization of the mitochondrial compartment resulting in apoptosis. These events were also associated with lysosomal membrane permeabilization and of caspase-8 activation, mediated by cathepsins and calpains, leading to Bid cleavage. Truncated tBid disrupts mitochondrial homeostasis and enhance apoptosis. We followed the induction of autophagy, marked by the formation of autophagosomes, by staining with acridine orange in cells exposed curcumin. At this concentration, only the early events of apoptosis (initial mitochondrial destabilization with any other manifestations) were detectable. Western blotting demonstrated the conversion of LC3-I to LC3-II (light chain 3), a marker of active autophagosome formation. We also found that the production of reactive oxygen species and formation of autophagosomes following curcumin treatment was almost completely blocked by N-acetylcystein, the mitochondrial specific antioxidants MitoQ10 and SKQ1, the calcium chelators, EGTA-AM or BAPTA-AM, and the mitochondrial calcium uniporter inhibitor, ruthenium red. Curcumin-induced autophagy failed to rescue all cells and most cells underwent type II cell death following the initial autophagic processes. All together, these data imply a fail-secure mechanism regulated by autophagy in the action of curcumin, suggesting a therapeutic potential for curcumin. Offering a novel and effective strategy for the treatment of malignant cells.

Identifiers

PMID27551451
PMCPMC4979459
OpenAlexW2521425438

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Registered trials

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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.