Evidence map›Paper›PMID 31557902›Full record

ReviewCells2019

Epigenetic Regulation of Inflammatory Cytokine-Induced Epithelial-To-Mesenchymal Cell Transition and Cancer Stem Cell Generation.

Georgios S Markopoulos, Eugenia Roupakia, Kenneth B Marcu, Evangelos Kolettas

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 78 citations in OpenAlex.

  1. Therapeutic responses toScience translational medicine · 2020
    Trial
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Observational
  11. Review
  12. Review
  13. Therapeutic Efficacy and Underlying Mechanisms of a Mannoglucan fromInternational journal of molecular sciences · 2024
    Article
  14. Factors Determining Epithelial-Mesenchymal Transition in Cancer Progression.International journal of molecular sciences · 2024
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  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

4 authors at 2 institutions in 2 countries.

Georgios S MarkopoulosLaboratory of Biology, School of Medicine, Faculty of Health Sciences, University of Ioannina, University Campus, 45110 Ioannina, Greece. gmarkop@cc.uoi.gr.ORCID 0000-0002-7700-7003
Eugenia RoupakiaLaboratory of Biology, School of Medicine, Faculty of Health Sciences, University of Ioannina, University Campus, 45110 Ioannina, Greece. ev.roupakia@gmail.com.
Kenneth B MarcuBiomedical Research Division, Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology, 45115 Ioannina, Greece. kenneth.marcu@stonybrook.edu.
Evangelos KolettasLaboratory of Biology, School of Medicine, Faculty of Health Sciences, University of Ioannina, University Campus, 45110 Ioannina, Greece. ekoletas@uoi.gr.
University of Ioannina · GRBiomedical Research Foundation of the Academy of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The neoplastic transformation of normal to metastatic cancer cells is a complex multistep process involving the progressive accumulation of interacting genetic and epigenetic changes that alter gene function and affect cell physiology and homeostasis. Epigenetic changes including DNA methylation, histone modifications and changes in noncoding RNA expression, and deregulation of epigenetic processes can alter gene expression during the multistep process of carcinogenesis. Cancer progression and metastasis through an 'invasion-metastasis cascade' involving an epithelial-to-mesenchymal cell transition (EMT), the generation of cancer stem cells (CSCs), invasion of adjacent tissues, and dissemination are fueled by inflammation, which is considered a hallmark of cancer. Chronic inflammation is generated by inflammatory cytokines secreted by the tumor and the tumor-associated cells within the tumor microenvironment. Inflammatory cytokine signaling initiates signaling pathways leading to the activation of master transcription factors (TFs) such as Smads, STAT3, and NF-κB. Moreover, the same inflammatory responses also activate EMT-inducing TF (EMT-TF) families such as Snail, Twist, and Zeb, and epigenetic regulators including DNA and histone modifying enzymes and micoRNAs, through complex interconnected positive and negative feedback loops to regulate EMT and CSC generation. Here, we review the molecular regulatory feedback loops and networks involved in inflammatory cytokine-induced EMT and CSC generation.

Indexed as

Neoplastic Stem CellsAnimalsCell Transformation, NeoplasticCytokinesEpigenesis, GeneticEpithelial-Mesenchymal TransitionFeedback, PhysiologicalGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansInflammation MediatorsSignal TransductionTranscription FactorsTumor MicroenvironmentCytokinesInflammation MediatorsTranscription Factorscancer stem cells (CSCs)epigenetic regulatorsepithelial-to-mesenchymal cell transition (EMT)feedback regulatory loopsinflammatory cytokine-induced EMT (ICI-EMT)inflammatory cytokinestranscription factors (TFs)tumor microenvironment (TME)

Identifiers

PMID31557902
PMCPMC6829508
OpenAlexW2975236857

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.