Evidence map›Paper›PMID 30080874›Full record

ArticlePloS one2018

The anticancer peptide RT53 induces immunogenic cell death.

Ewa Pasquereau-Kotula, Justine Habault, Guido Kroemer, Jean-Luc Poyet

Abstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
–field-weighted citation impact
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

38 citing papers in PubMed.

  1. Review
  2. Immunobiological mechanisms of action of oncolytic peptides.Journal for immunotherapy of cancer · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Killing ofMicroorganisms · 2024
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Peptide cargo administration: current state and applications.Applied microbiology and biotechnology · 2023
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Role of HMGB1 in Cutaneous Melanoma: State of the Art.International journal of molecular sciences · 2022
    Review
  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

4 authors.

Ewa Pasquereau-KotulaINSERM UMRS1160, Institut Universitaire d'Hématologie, Hôpital Saint-Louis, Paris, France.
Justine HabaultINSERM UMRS1160, Institut Universitaire d'Hématologie, Hôpital Saint-Louis, Paris, France.ORCID 0000-0001-6375-6428
Guido KroemerEquipe 11 labellisée par la Ligue Nationale contre le Cancer, Center de Recherche des Cordeliers, Paris, France.
Jean-Luc PoyetINSERM UMRS1160, Institut Universitaire d'Hématologie, Hôpital Saint-Louis, Paris, France.ORCID 0000-0002-3747-255X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In recent years, immunogenic cell death (ICD) has emerged as a revolutionary concept in the development of novel anticancer therapies. This particular form of cell death is able, through the spatiotemporally defined emission of danger signals by the dying cell, to induce an effective antitumor immune response, allowing the immune system to recognize and eradicate malignant cells. To date, only a restricted number of chemotherapeutics can trigger ICD of cancer cells. We previously reported that a peptide, called RT53, spanning the heptad leucine repeat region of the survival protein AAC-11 fused to a penetrating sequence, selectively induces cancer cell death in vitro and in vivo. Interestingly, B16F10 melanoma cells treated by RT53 were able to mediate anticancer effects in a tumor vaccination model. Stimulated by this observation, we investigated whether RT53 might mediate ICD of cancer cells. Here, we report that RT53 treatment induces all the hallmarks of immunogenic cell death, as defined by the plasma membrane exposure of calreticulin, release of ATP and the exodus of high-mobility group box 1 protein (HMGB1) from dying cancer cells, through a non-regulated, membranolytic mode of action. In a prophylactic mouse model, vaccination with RT53-treated fibrosarcomas prevented tumor growth at the challenge site. Finally, local intratumoral injection of RT53 into established cancers led to tumor regression together with T-cell infiltration and the mounting of an inflammatory response in the treated animals. Collectively, our results strongly suggest that RT53 can induce bona fide ICD of cancer cells and illustrate its potential use as a novel antitumor and immunotherapeutic strategy.

Indexed as

Amino Acid SequenceAnimalsAntineoplastic AgentsApoptosis Regulatory ProteinsCell DeathCell Line, TumorCell-Penetrating PeptidesHL-60 CellsHumansJurkat CellsMiceMice, Inbred C57BLNuclear ProteinsPeptide FragmentsPeptidesRecombinant Fusion ProteinsAntineoplastic AgentsAPI5 protein, humanApoptosis Regulatory ProteinsCell-Penetrating PeptidesNuclear ProteinspenetratinPeptide FragmentsPeptidesRecombinant Fusion ProteinsRT53 peptide

Identifiers

PMID30080874
PMCPMC6078289

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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.