Evidence map›Paper›PMID 33117715›Full record

ReviewFrontiers in oncology2020

The Double-Edge Sword of Autophagy in Cancer: From Tumor Suppression to Pro-tumor Activity.

Rodolfo Chavez-Dominguez, Mario Perez-Medina, Jose S Lopez-Gonzalez, Miriam Galicia-Velasco, Dolores Aguilar-Cazares

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
181citing papers in PubMed, 3 pooled it
22.5field-weighted citation impact, top 1% 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

181 citing papers in PubMed, 3 syntheses or guidelines pooled it, 298 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Review
  6. Article
  7. Autophagy in Melanoma: Molecular Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2026
    Review
  8. Article
  9. Review
  10. Autophagy in Ovarian Cancer, an Opportunity or an Additional Threat?International journal of molecular sciences · 2026
    Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

121 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

5 authors at 2 institutions in 1 country.

Rodolfo Chavez-DominguezDepartamento de Enfermedades Cronico-Degenerativas, Instituto Nacional de Enfermedades Respiratorias "Ismael Cosio Villegas", Mexico City, Mexico.
Mario Perez-MedinaDepartamento de Enfermedades Cronico-Degenerativas, Instituto Nacional de Enfermedades Respiratorias "Ismael Cosio Villegas", Mexico City, Mexico.
Jose S Lopez-GonzalezDepartamento de Enfermedades Cronico-Degenerativas, Instituto Nacional de Enfermedades Respiratorias "Ismael Cosio Villegas", Mexico City, Mexico.
Miriam Galicia-VelascoDepartamento de Enfermedades Cronico-Degenerativas, Instituto Nacional de Enfermedades Respiratorias "Ismael Cosio Villegas", Mexico City, Mexico.
Dolores Aguilar-CazaresDepartamento de Enfermedades Cronico-Degenerativas, Instituto Nacional de Enfermedades Respiratorias "Ismael Cosio Villegas", Mexico City, Mexico.
Instituto Nacional de Enfermedades Respiratorias · MXUniversidad Nacional Autónoma de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During tumorigenesis, cancer cells are exposed to a wide variety of intrinsic and extrinsic stresses that challenge homeostasis and growth. Cancer cells display activation of distinct mechanisms for adaptation and growth even in the presence of stress. Autophagy is a catabolic mechanism that aides in the degradation of damaged intracellular material and metabolite recycling. This activity helps meet metabolic needs during nutrient deprivation, genotoxic stress, growth factor withdrawal and hypoxia. However, autophagy plays a paradoxical role in tumorigenesis, depending on the stage of tumor development. Early in tumorigenesis, autophagy is a tumor suppressor via degradation of potentially oncogenic molecules. However, in advanced stages, autophagy promotes the survival of tumor cells by ameliorating stress in the microenvironment. These roles of autophagy are intricate due to their interconnection with other distinct cellular pathways. In this review, we present a broad view of the participation of autophagy in distinct phases of tumor development. Moreover, autophagy participation in important cellular processes such as cell death, metabolic reprogramming, metastasis, immune evasion and treatment resistance that all contribute to tumor development, is reviewed. Finally, the contribution of the hypoxic and nutrient deficient tumor microenvironment in regulation of autophagy and these hallmarks for the development of more aggressive tumors is discussed.

Indexed as

autophagycarcinogenesiscell deathchemotherapy and targeted therapy resistanceimmune evasionmetabolic reprogramingmetastasistumor microenvironment

Identifiers

PMID33117715
PMCPMC7575731
OpenAlexW3091837166

What OpenQuestion holds

Textmetadata
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.