Evidence map›Paper›PMID 26338963›Full record

ArticleOncotarget2015

Capsaicin triggers immunogenic PEL cell death, stimulates DCs and reverts PEL-induced immune suppression.

Marisa Granato, Maria Saveria Gilardini Montani, Mariarosari Filardi, Alberto Faggioni, Mara Cirone

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Review
  3. Capsaicin: beyond TRPV1.Frontiers in nutrition · 2025
    Review
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  8. Article
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  14. Neuropeptides in gut-brain axis and their influence on host immunity and stress.Computational and structural biotechnology journal · 2020
    Review
  15. Article
  16. Article
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  18. Review
  19. Reactivation of mutant p53 by capsaicin, the major constituent of peppers.Journal of experimental & clinical cancer research : CR · 2016
    Article
  20. 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

5 authors at 1 institution in 1 country.

Marisa GranatoDepartment of Experimental Medicine, Sapienza University of Rome, 00161 Rome, Italy.
Maria Saveria Gilardini MontaniDepartment of Experimental Medicine, Sapienza University of Rome, 00161 Rome, Italy.
Mariarosari FilardiDepartment of Experimental Medicine, Sapienza University of Rome, 00161 Rome, Italy.
Alberto FaggioniDepartment of Experimental Medicine, Sapienza University of Rome, 00161 Rome, Italy.
Mara CironeDepartment of Experimental Medicine, Sapienza University of Rome, 00161 Rome, Italy.
Sapienza University of Rome · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Capsaicin, the pungent alkaloid of red pepper has been extensively studied for its many properties, especially the anti-inflammatory and anti-oxidant ones. It binds to vanilloid receptor 1, although it has been reported to be able to mediate some effects independently of its receptor. Another important property of Capsaicin is the anticancer activity against highly malignant tumors, alone or in combination with other chemotherapeutic agents. In this study, we found that Capsaicin induced an apoptotic cell death in PEL cells correlated with the inhibition of STAT3. STAT3 pathway, constitutively activated in PEL cells, is essential for their survival. By STAT3 de-phosphorylation, Capsaicin reduced the Mcl-1 expression level and this could represent one of the underlying mechanisms leading to the Capsaicin-mediated cell death and autophagy induction. Next, by pharmacological or genetic inhibition, we found that autophagy played a pro-survival role, suggesting that its inhibition could be exploited to increase the Capsaicin cytotoxic effect against PEL cells. Finally, we show that Capsaicin induced DAMP exposure, as for an immunogenic cell death, directly promoted DC activation and, more importantly, that it counteracted the immune-suppression, in terms of DC differentiation, mediated by the PEL released factors.

Indexed as

ApoptosisAutophagyBlotting, WesternCalreticulinCapsaicinCaspase 3Cell DifferentiationCell Line, TumorCell SurvivalCulture Media, ConditionedDendritic CellsDose-Response Relationship, DrugHSP90 Heat-Shock ProteinsHumansLymphoma, Primary EffusionMonocytesCalreticulinCapsaicinCaspase 3Culture Media, ConditionedHSP90 Heat-Shock ProteinsMCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinSTAT3 Transcription FactorCapsaicinDCsimmunogenic cell deathPELSTAT3

Identifiers

PMID26338963
PMCPMC4745745
OpenAlexW1766967506

What OpenQuestion 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 OpenQuestion graph.