Evidence map›Paper›PMID 38398197›Full record

ReviewCancers2024

Contribution of Autophagy to Epithelial Mesenchymal Transition Induction during Cancer Progression.

Raffaele Strippoli, Reyhaneh Niayesh-Mehr, Maryam Adelipour, Arezoo Khosravi, Marco Cordani, Ali Zarrabi, Abdolamir Allameh

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
8.9field-weighted citation impact, top 2% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. [Inhibition of BRD4 promotes migration of esophageal squamous cell carcinoma cells with low ACC1 expression].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Frontiers in pharmacology · 2024
    Article
  18. Review
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

7 authors at 6 institutions in 5 countries.

Raffaele StrippoliDepartment of Molecular Medicine, Sapienza University of Rome, 00161 Rome, Italy.ORCID 0000-0003-3483-8381
Reyhaneh Niayesh-MehrDepartment of Clinical Biochemistry, Faculty of Medical Science, Tarbiat Modares University, Tehran P.O. Box 14115-331, Iran.
Maryam AdelipourDepartment of Clinical Biochemistry, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz 61357-15794, Iran.
Arezoo KhosraviDepartment of Genetics and Bioengineering, Faculty of Engineering and Natural Sciences, Istanbul Okan University, Istanbul 34959, Türkiye.ORCID 0009-0006-6654-4133
Marco CordaniDepartment of Biochemistry and Molecular Biology, Faculty of Biological Sciences, Complutense University of Madrid, 28040 Madrid, Spain.ORCID 0000-0001-9342-4862
Ali ZarrabiDepartment of Biomedical Engineering, Faculty of Engineering and Natural Sciences, Istinye University, Istanbul 34396, Türkiye.ORCID 0000-0003-0391-1769
Abdolamir AllamehDepartment of Clinical Biochemistry, Faculty of Medical Science, Tarbiat Modares University, Tehran P.O. Box 14115-331, Iran.ORCID 0000-0003-0757-9572
Tarbiat Modares University · IRAhvaz Jundishapur University of Medical Sciences · IRIstinye University · TRIstituto Nazionale per le Malattie Infettive Lazzaro Spallanzani · ITOkan University · TRUniversidad Complutense de Madrid · ES

Funding

Italian ministry of University and and research (miur) P2022XZKBM
6 · The paper itself

Abstract

Epithelial Mesenchymal Transition (EMT) is a dedifferentiation process implicated in many physio-pathological conditions including tumor transformation. EMT is regulated by several extracellular mediators and under certain conditions it can be reversible. Autophagy is a conserved catabolic process in which intracellular components such as protein/DNA aggregates and abnormal organelles are degraded in specific lysosomes. In cancer, autophagy plays a controversial role, acting in different conditions as both a tumor suppressor and a tumor-promoting mechanism. Experimental evidence shows that deep interrelations exist between EMT and autophagy-related pathways. Although this interplay has already been analyzed in previous studies, understanding mechanisms and the translational implications of autophagy/EMT need further study. The role of autophagy in EMT is not limited to morphological changes, but activation of autophagy could be important to DNA repair/damage system, cell adhesion molecules, and cell proliferation and differentiation processes. Based on this, both autophagy and EMT and related pathways are now considered as targets for cancer therapy. In this review article, the contribution of autophagy to EMT and progression of cancer is discussed. This article also describes the multiple connections between EMT and autophagy and their implication in cancer treatment.

Indexed as

autophagycell adhesion moleculescell deathcell proliferationdifferentiationepithelial mesenchymal transition

Identifiers

PMID38398197
PMCPMC10886827
OpenAlexW4391883337

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.