Evidence map›Paper›PMID 40346781›Full record

ReviewFEBS letters2025

Decoding the dual role of autophagy in cancer through transcriptional and epigenetic regulation.

Young Suk Yu, Ik Soo Kim, Sung Hee Baek

Abstract readReview
In one paragraph

Review in FEBS letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Autophagy in Melanoma: Molecular Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Autophagy: A Double-Edged Sword in the Aging ofInternational journal of molecular sciences · 2026
    Review
  5. Article
  6. Review
  7. Microbial cell (Graz, Austria) · 2026
    Article
  8. Review
  9. Review
  10. Review
  11. 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

3 authors.

Young Suk YuCreative Research Initiatives Center for Epigenetic Code and Diseases, School of Biological Sciences, Seoul National University, Seoul, Korea.
Ik Soo KimDepartment of Microbiology, Gachon University College of Medicine, Incheon, South Korea.
Sung Hee BaekCreative Research Initiatives Center for Epigenetic Code and Diseases, School of Biological Sciences, Seoul National University, Seoul, Korea.ORCID https://orcid.org/0000-0002-0588-8243

Funding

National Research Foundation of Korea 2017R1A3B1023387National Research Foundation of Korea 2021R1A5A2030333National Research Foundation of Korea 2021R1C1C2010332
6 · The paper itself

Abstract

Autophagy is a conserved catabolic process that is essential for maintaining cellular homeostasis by degrading and recycling damaged organelles and misfolded proteins. In cancer, autophagy exhibits a context-dependent dual role: In early stages, autophagy acts as a tumor suppressor by preserving genomic integrity and limiting oxidative stress. In advanced stages, autophagy supports tumor progression by facilitating metabolic adaptation, therapy resistance, immune evasion, and metastasis. This review highlights the molecular mechanisms underlying this dual function and focuses on the transcriptional and epigenetic regulation of autophagy in cancer cells. Key transcription factors, including the MiT/TFE family, FOXO family, and p53, as well as additional regulators, are discussed in the context of stress-responsive pathways mediated by mTORC1 and AMPK. A deeper understanding of the transcriptional and epigenetic regulation of autophagy in cancer is crucial for developing context-specific therapeutic strategies to either promote or inhibit autophagy depending on the cancer stage, thereby improving clinical outcomes in cancer treatment.

Indexed as

AutophagyEpigenesis, GeneticGene Expression Regulation, NeoplasticNeoplasmsTranscription, GeneticAnimalsHumansautophagycancerepigeneticslysosometranscription factor

Identifiers

PMID40346781
PMCPMC12375893

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.