Evidence mapPaperPMID 35054987Full record

ReviewInternational journal of molecular sciences2022

The Epithelial-Mesenchymal Transition at the Crossroads between Metabolism and Tumor Progression.

Monica Fedele, Riccardo Sgarra, Sabrina Battista, Laura Cerchia, Guidalberto Manfioletti

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
16.8field-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

96 citing papers in PubMed, 1 synthesis or guideline pooled it, 166 citations in OpenAlex.

  1. Interaction of HIF-1a with various cell death pathways in tumor immune microenvironment (TIME).Apoptosis : an international journal on programmed cell death · 2026
    Pooled it
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  3. Review
  4. Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026
    Review
  5. Article
  6. Article
  7. Metabolic reprogramming and plasticity of cancer stem cells.Frontiers in cell and developmental biology · 2026
    Review
  8. Article
  9. Review
  10. RBMX2 linkseLife · 2025
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

36 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.

Monica FedeleNational Research Council (CNR), Institute of Experimental Endocrinology and Oncology "G. Salvatore" (IEOS), 80131 Naples, Italy.ORCID 0000-0002-9171-1312
Riccardo SgarraDepartment of Life Sciences, University of Trieste, 34127 Trieste, Italy.
Sabrina BattistaNational Research Council (CNR), Institute of Experimental Endocrinology and Oncology "G. Salvatore" (IEOS), 80131 Naples, Italy.
Laura CerchiaNational Research Council (CNR), Institute of Experimental Endocrinology and Oncology "G. Salvatore" (IEOS), 80131 Naples, Italy.ORCID 0000-0002-7633-7932
Guidalberto ManfiolettiDepartment of Life Sciences, University of Trieste, 34127 Trieste, Italy.ORCID 0000-0001-7913-2601
Institute for Experimental Endocrinology and Oncology · ITUniversity of Trieste · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transition between epithelial and mesenchymal phenotype is emerging as a key determinant of tumor cell invasion and metastasis. It is a plastic process in which epithelial cells first acquire the ability to invade the extracellular matrix and migrate into the bloodstream via transdifferentiation into mesenchymal cells, a phenomenon known as epithelial-mesenchymal transition (EMT), and then reacquire the epithelial phenotype, the reverse process called mesenchymal-epithelial transition (MET), to colonize a new organ. During all metastatic stages, metabolic changes, which give cancer cells the ability to adapt to increased energy demand and to withstand a hostile new environment, are also important determinants of successful cancer progression. In this review, we describe the complex interaction between EMT and metabolism during tumor progression. First, we outline the main connections between the two processes, with particular emphasis on the role of cancer stem cells and LncRNAs. Then, we focus on some specific cancers, such as breast, lung, and thyroid cancer.

Indexed as

Energy MetabolismEpithelial-Mesenchymal TransitionAnimalsBiomarkersBiomarkers, TumorDisease ManagementDisease ProgressionDisease SusceptibilityDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansMetabolic Networks and PathwaysMolecular Targeted TherapyNeoplasmsNeoplastic Stem CellsOrgan SpecificityBiomarkersBiomarkers, TumorRNA, Long NoncodingTranscription Factorsbreast cancercancerepithelial–mesenchymal transition (EMT)lung cancermetabolic rewiringmetabolismthyroid cancertumor progressionWarburg effect

Identifiers

PMID35054987
PMCPMC8776206
OpenAlexW4205537120

What Socratic 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 Socratic graph.