Evidence map›Paper›PMID 25590798›Full record

ReviewRedox biology2015

Interplay between ROS and autophagy in cancer cells, from tumor initiation to cancer therapy.

Laura Poillet-Perez, Gilles Despouy, Régis Delage-Mourroux, Michaël Boyer-Guittaut

Abstract readReview
In one paragraph

Review in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 243 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
243citing papers in PubMed, 1 pooled it
–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

243 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  19. Autophagy: The convergence point of aging and cancer.Biochemistry and biophysics reports · 2025
    Review
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183 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

4 authors.

Laura Poillet-PerezUniversité de Franche-Comté, Laboratoire de Biochimie, EA3922 «Estrogènes, Expression Génique et Pathologies du Système Nerveux Central», SFR IBCT FED4234, UFR Sciences et Techniques, 16 Route de Gray, 25030 Besançon Cedex, France.
Gilles DespouyUniversité de Franche-Comté, Laboratoire de Biochimie, EA3922 «Estrogènes, Expression Génique et Pathologies du Système Nerveux Central», SFR IBCT FED4234, UFR Sciences et Techniques, 16 Route de Gray, 25030 Besançon Cedex, France.
Régis Delage-MourrouxUniversité de Franche-Comté, Laboratoire de Biochimie, EA3922 «Estrogènes, Expression Génique et Pathologies du Système Nerveux Central», SFR IBCT FED4234, UFR Sciences et Techniques, 16 Route de Gray, 25030 Besançon Cedex, France.
Michaël Boyer-GuittautUniversité de Franche-Comté, Laboratoire de Biochimie, EA3922 «Estrogènes, Expression Génique et Pathologies du Système Nerveux Central», SFR IBCT FED4234, UFR Sciences et Techniques, 16 Route de Gray, 25030 Besançon Cedex, France. Electronic address: michael.boyer-guittaut@univ-fcomte.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer formation is a complex and highly regulated multi-step process which is highly dependent of its environment, from the tissue to the patient. This complexity implies the development of specific treatments adapted to each type of tumor. The initial step of cancer formation requires the transformation of a healthy cell to a cancer cell, a process regulated by multiple intracellular and extracellular stimuli. The further steps, from the anarchic proliferation of cancer cells to form a primary tumor to the migration of cancer cells to distant organs to form metastasis, are also highly dependent of the tumor environment but of intracellular molecules and pathways as well. In this review, we will focus on the regulatory role of reactive oxygen species (ROS) and autophagy levels during the course of cancer development, from cellular transformation to the formation of metastasis. These data will allow us to discuss the potential of this molecule or pathway as putative future therapeutic targets.

Indexed as

Gene Expression Regulation, NeoplasticAMP-Activated Protein KinasesAntineoplastic AgentsApoptosis Regulatory ProteinsAutophagyAutophagy-Related Protein-1 HomologAutophagy-Related ProteinsBeclin-1Cell Transformation, NeoplasticCysteine EndopeptidasesHumansIntracellular Signaling Peptides and ProteinsKelch-Like ECH-Associated Protein 1Lymphatic MetastasisMembrane ProteinsMitochondriaAMP-Activated Protein KinasesAntineoplastic AgentsApoptosis Regulatory ProteinsATG4A protein, humanAutophagy-Related Protein-1 HomologAutophagy-Related ProteinsBeclin-1BECN1 protein, humanCysteine EndopeptidasesIntracellular Signaling Peptides and ProteinsKEAP1 protein, humanKelch-Like ECH-Associated Protein 1Membrane ProteinsProtein Serine-Threonine KinasesReactive Oxygen SpeciesULK1 protein, humanAntioxidantAutophagyCancerMitochondriaMitophagyROS

Identifiers

PMID25590798
PMCPMC4803791

What OpenQuestion holds

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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.