Evidence map›Paper›PMID 33159487›Full record

ArticleJournal of cellular and molecular medicine2020

Thidiazuron decreases epithelial-mesenchymal transition activity through the NF-kB and PI3K/AKT signalling pathways in breast cancer.

Peramaiyan Rajendran, Rebai Ben Ammar, Fatma J Al-Saeedi, Maged Elsayed Mohamed, Mih Islam, Saeed Y Al-Ramadan

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Understanding the role of TNFR2 signaling in the tumor microenvironment of breast cancer.Journal of experimental & clinical cancer research : CR · 2024
    Review
  5. Review
  6. Review
  7. Article
  8. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Journal of personalized medicine · 2021
    Article
  14. 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

6 authors at 4 institutions in 4 countries.

Peramaiyan RajendranDepartment of Biological Sciences, College of Science, King Faisal University, Al-Ahsa, Saudi Arabia.ORCID 0000-0001-6354-4388
Rebai Ben AmmarDepartment of Biological Sciences, College of Science, King Faisal University, Al-Ahsa, Saudi Arabia.ORCID 0000-0002-9454-6295
Fatma J Al-SaeediDepartment of Nuclear Medicine, Faculty of Medicine, Kuwait University, Safat, Kuwait.
Maged Elsayed MohamedDepartment of Pharmaceutical Sciences, College of Clinical Pharmacy, King Faisal University, Al-Ahsaa, Saudi Arabia.
Mih IslamDepartment of Biological Sciences, College of Science, King Faisal University, Al-Ahsa, Saudi Arabia.
Saeed Y Al-RamadanDepartment of Anatomy, College of Veterinary Medicine, King Faisal University, Al-Ahsa, Saudi Arabia.
King Faisal University · SACenter of Biotechnogy of Borj Cédria · TNKuwait University · KWZagazig University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is the major type among the women population globally. The treatment of cancer metastasis has made modest progress due to multiple factors. Thidiazuron (TDZ) is a novel plant growth regulator that has been shown to have anticancer effects. Therefore, we explored the anti-metastatic potentials of TDZ in cell lines by assessing its potential to suppress the epithelial-mesenchymal transition (EMT). We pretreated the BEAS-2B and breast cancer (MDA-MB-231) cells with TDZ and deliberated alteration in a cell viability, mammosphere, migration, NF-кB signalling, PI3K/AKT signalling and matrix metalloproteinase (MMP) expression and analysed the EMT induction by TGF-β/TNF-α-stimulated BEAS-2B cells. Treatment with TDZ (5-50 μmol) diminished the migration and invasion of the extremely metastatic MDA-MB-231 cells. Additionally, TDZ treatment led to down-regulation of uPAR, uPA, VEGF and MMP-2/-9 expression and up-regulation of TIMP-1/2 expression in these cells. Furthermore, TDZ treatment blocked invasion and EMT in non-tumorigenic BEAS-2B epithelial cells stimulated with TGF-β/TNF-α.TDZ prevents EMT and may thus block metastasis of breast cancer cells.

Indexed as

BiomarkersBreast NeoplasmsCaspase 3Cell Line, TumorCell MovementCell SurvivalDNA FragmentationEpithelial-Mesenchymal TransitionFemaleHumansImmunohistochemistryMatrix MetalloproteinasesNF-kappa BPhenylurea CompoundsPhosphatidylinositol 3-KinasesPoly(ADP-ribose) PolymerasesBiomarkersCaspase 3Matrix MetalloproteinasesNF-kappa BPhenylurea CompoundsPhosphatidylinositol 3-KinasesPoly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-aktThiadiazolesthidiazuronbreast cancerepithelial-mesenchymal transitionmatrix metalloproteinasemetastasisThidiazuron

Identifiers

PMID33159487
PMCPMC7754050
OpenAlexW3095107406

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.