Evidence map›Paper›PMID 25328887›Full record

ReviewBioMed research international2014

Tumor suppression and promotion by autophagy.

Yenniffer Ávalos, Jimena Canales, Roberto Bravo-Sagua, Alfredo Criollo, Sergio Lavandero, Andrew F G Quest

Registry-linked trialOpen access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04729855 (Association of Autophagy-related Genes ,LncRNA and SNPs With Colorectal Cancer in Egyptian Population), which is not on this map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
12.0field-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.

NCT04729855 completednot on this mapstarted 2022, after this paper: background citation

Association of Autophagy-related Genes ,LncRNA and SNPs With Colorectal Cancer in Egyptian Population

TypeobservationalSponsorEsraa Hassan,MDRan2022 to 2024Enrolled60ConditionsColo-rectal CancerArmsPBMCs and Tissue expression of HOTTIP ,EIF4EBP1 and serum SNP HOTTIP rs1859168
3 · Its place in the literature

Who cites it

111 citing papers in PubMed, 187 citations in OpenAlex.

  1. Article
  2. Autophagy in Melanoma: Molecular Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. International journal of molecular sciences · 2025
    Article
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  10. Review
  11. Article
  12. Review
  13. Article
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  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

51 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

6 authors at 2 institutions in 2 countries.

Yenniffer ÁvalosLaboratory of Cellular Communication, Advanced Center for Chronic Diseases (ACCDiS) and Center for Molecular Studies of the Cell, Program in Cell and Molecular Biology, Biomedical Sciences Institute (ICBM), Faculty of Medicine, University of Chile, 8380492 Santiago, Chile ; Laboratory of Molecular Signal Transduction, Advanced Center for Chronic Diseases (ACCDiS) and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences & Faculty of Medicine, University of Chile, 8380492 Santiago, Chile.
Jimena CanalesLaboratory of Cellular Communication, Advanced Center for Chronic Diseases (ACCDiS) and Center for Molecular Studies of the Cell, Program in Cell and Molecular Biology, Biomedical Sciences Institute (ICBM), Faculty of Medicine, University of Chile, 8380492 Santiago, Chile.
Roberto Bravo-SaguaLaboratory of Cellular Communication, Advanced Center for Chronic Diseases (ACCDiS) and Center for Molecular Studies of the Cell, Program in Cell and Molecular Biology, Biomedical Sciences Institute (ICBM), Faculty of Medicine, University of Chile, 8380492 Santiago, Chile ; Laboratory of Molecular Signal Transduction, Advanced Center for Chronic Diseases (ACCDiS) and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences & Faculty of Medicine, University of Chile, 8380492 Santiago, Chile.ORCID 0000-0001-8873-8699
Alfredo CriolloResearch Institute of Dental Science, Faculty of Dentistry, University of Chile, 8380492 Santiago, Chile.
Sergio LavanderoLaboratory of Molecular Signal Transduction, Advanced Center for Chronic Diseases (ACCDiS) and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences & Faculty of Medicine, University of Chile, 8380492 Santiago, Chile ; Department of Internal Medicine, Cardiology Division, University of Texas Southwestern Medical Center, Dallas, TX 75235, USA.ORCID 0000-0003-4258-1483
Andrew F G QuestLaboratory of Cellular Communication, Advanced Center for Chronic Diseases (ACCDiS) and Center for Molecular Studies of the Cell, Program in Cell and Molecular Biology, Biomedical Sciences Institute (ICBM), Faculty of Medicine, University of Chile, 8380492 Santiago, Chile.
Advanced Center for Chronic Diseases · CLUniversity of Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a highly regulated catabolic process that involves lysosomal degradation of proteins and organelles, mostly mitochondria, for the maintenance of cellular homeostasis and reduction of metabolic stress. Problems in the execution of this process are linked to different pathological conditions, such as neurodegeneration, aging, and cancer. Many of the proteins that regulate autophagy are either oncogenes or tumor suppressor proteins. Specifically, tumor suppressor genes that negatively regulate mTOR, such as PTEN, AMPK, LKB1, and TSC1/2 stimulate autophagy while, conversely, oncogenes that activate mTOR, such as class I PI3K, Ras, Rheb, and AKT, inhibit autophagy, suggesting that autophagy is a tumor suppressor mechanism. Consistent with this hypothesis, the inhibition of autophagy promotes oxidative stress, genomic instability, and tumorigenesis. Nevertheless, autophagy also functions as a cytoprotective mechanism under stress conditions, including hypoxia and nutrient starvation, that promotes tumor growth and resistance to chemotherapy in established tumors. Here, in this brief review, we will focus the discussion on this ambiguous role of autophagy in the development and progression of cancer.

Indexed as

AutophagyModels, BiologicalAnimalsHumansNeoplasmsTumor Suppressor ProteinsTumor Suppressor Proteins

Identifiers

PMID25328887
PMCPMC4189854
OpenAlexW1991903498

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.