Evidence mapPaperPMID 29729928Full record

ArticleToxicology2018

Inhibition of tumorigenesis by peroxisome proliferator-activated receptor (PPAR)-dependent cell cycle blocks in human skin carcinoma cells.

Michael G Borland, Ellen M Kehres, Christina Lee, Ashley L Wagner, Brooke E Shannon, Prajakta P Albrecht, Bokai Zhu, Frank J Gonzalez, Jeffrey M Peters

Open access · greenAbstract read
In one paragraph

Article in Toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Trial
  2. Transcriptional and functional regulation of cell cycle and UV response by PPARβ in human skin epidermal cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Self-regulation of the inflammatory response by peroxisome proliferator-activated receptors.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Review
  12. Article
  13. 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

9 authors at 4 institutions in 1 country.

Michael G BorlandDepartment of Veterinary and Biomedical Sciences, The Center of Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, PA 16802, USA; Department of Chemistry & Biochemistry, Bloomsburg University of Pennsylvania, Bloomsburg, PA 17815, USA.
Ellen M KehresDepartment of Chemistry & Biochemistry, Bloomsburg University of Pennsylvania, Bloomsburg, PA 17815, USA.
Christina LeeDepartment of Veterinary and Biomedical Sciences, The Center of Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, PA 16802, USA.
Ashley L WagnerDepartment of Chemistry & Biochemistry, Bloomsburg University of Pennsylvania, Bloomsburg, PA 17815, USA.
Brooke E ShannonDepartment of Chemistry & Biochemistry, Bloomsburg University of Pennsylvania, Bloomsburg, PA 17815, USA.
Prajakta P AlbrechtDepartment of Veterinary and Biomedical Sciences, The Center of Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, PA 16802, USA.
Bokai ZhuDepartment of Veterinary and Biomedical Sciences, The Center of Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, PA 16802, USA.
Frank J GonzalezLaboratory of Metabolism, National Cancer Institute, Bethesda, MD 20892, USA.
Jeffrey M PetersDepartment of Veterinary and Biomedical Sciences, The Center of Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, PA 16802, USA. Electronic address: jmp21@psu.edu.
Pennsylvania State University · USUniversity of Pennsylvania · USBloomsburg University · USNational Cancer Institute · US

Funding

Xenobiotic receptorsZIABC005562 · DIVISION OF BASIC SCIENCES - NCI · 2025 to 2025
$2.6M
NCI NIH HHS R01 CA124533NCI NIH HHS R01 CA140369
6 · The paper itself

Abstract

To examine the functional role of peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) and PPARγ in skin cancer, stable cell lines were created in the A431 human squamous cell carcinoma cell line. Expression of PPAR target genes was greatly enhanced in response to ligand activation of PPARβ/δ or PPARγ in A431 cells expressing these receptors. PPARβ/δ expression blocked the cell cycle at the G2/M phase, and this effect was increased by ligand activation. Ligand activation of PPARβ/δ markedly inhibited clonogenicity as compared to vehicle-treated controls. Similarly, ligand activation of PPARγ in A431 cells expressing PPARγ resulted in reduced clonogenicity. Expression of either PPARβ/δ or PPARγ markedly reduced tumor volume in ectopic xenografts, while ligand activation of these receptors had little further influence on tumor volume. Collectively, these studies demonstrate that stable expression and activation of PPARβ/δ or PPARγ in A431 cells led to reduced tumorigenicity. Importantly, PPAR expression or ligand activation had major impacts on clonogenicity and/or tumor volume. Thus, PPARβ/δ or PPARγ could be therapeutically targeted for the treatment of squamous cell carcinomas.

Indexed as

AnimalsCarcinogenesisCarcinoma, Squamous CellCell CycleCell Cycle CheckpointsCell Line, TumorFemaleHumansMice, NudePPAR-betaPPAR deltaSkin NeoplasmsXenograft Model Antitumor AssaysPPAR-betaPPAR deltaCarcinomaCell cyclePPARβ/δPPARγProliferationSkin

Identifiers

PMID29729928
PMCPMC6026558
OpenAlexW2799604816

What Socratic holds

Textmetadata
LicenceTDM
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.