Evidence map›Paper›PMID 31010154›Full record

ReviewInternational journal of molecular sciences2019

The Crosstalk Between Cell Adhesion and Cancer Metabolism.

Bárbara Sousa, Joana Pereira, Joana Paredes

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Metabolic Cross Talk in the Tumor Microenvironment.Cancer treatment and research · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. [Extracellular Matrix Stiffness Induces Mitochondrial Morphological Heterogeneity via AMPK Activation].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024
    Article
  18. Article
  19. Review
  20. 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 at 1 institution in 1 country.

Bárbara SousaIpatimup-Institute of Molecular Pathology and Immunology of the University of Porto, 4200-135 Porto, Portugal. bsousa@ipatimup.pt.ORCID 0000-0002-0990-022X
Joana PereiraIpatimup-Institute of Molecular Pathology and Immunology of the University of Porto, 4200-135 Porto, Portugal. jspereira@ipatimup.pt.
Joana ParedesIpatimup-Institute of Molecular Pathology and Immunology of the University of Porto, 4200-135 Porto, Portugal. jparedes@ipatimup.pt.
Universidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells preferentially use aerobic glycolysis over mitochondria oxidative phosphorylation for energy production, and this metabolic reprogramming is currently recognized as a hallmark of cancer. Oncogenic signaling frequently converges with this metabolic shift, increasing cancer cells' ability to produce building blocks and energy, as well as to maintain redox homeostasis. Alterations in cell-cell and cell-extracellular matrix (ECM) adhesion promote cancer cell invasion, intravasation, anchorage-independent survival in circulation, and extravasation, as well as homing in a distant organ. Importantly, during this multi-step metastatic process, cells need to induce metabolic rewiring, in order to produce the energy needed, as well as to impair oxidative stress. Although the individual implications of adhesion molecules and metabolic reprogramming in cancer have been widely explored over the years, the crosstalk between cell adhesion molecular machinery and metabolic pathways is far from being clearly understood, in both normal and cancer contexts. This review summarizes our understanding about the influence of cell-cell and cell-matrix adhesion in the metabolic behavior of cancer cells, with a special focus concerning the role of classical cadherins, such as Epithelial (E)-cadherin and Placental (P)-cadherin.

Indexed as

AnimalsBiomechanical PhenomenaCell AdhesionCell-Matrix JunctionsDisease ProgressionEpithelial-Mesenchymal TransitionHumansNeoplasmsadhesioncadherincancercancer stem cellsECMmetabolism

Identifiers

PMID31010154
PMCPMC6515343
OpenAlexW2937345593

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.