Evidence map›Paper›PMID 34402100›Full record

ArticleJournal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology2021

Fatty acid synthase mediates high glucose-induced EGFR activation in oral dysplastic keratinocytes.

David J Wisniewski, Tao Ma, Abraham Schneider

Open access · greenAbstract read
In one paragraph

Article in Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 43% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. A review on diabetes and oral cancer: Molecular links and implications.Molecular biology research communications · 2025
    Review
  5. Inhibitory Effects of the Polyphenols from the Root ofMolecules (Basel, Switzerland) · 2024
    Article
  6. Glucose upregulates amphiregulin in oral dysplastic keratinocytes: A potential role in diabetes-associated oral carcinogenesis.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2023
    Article
  7. Article
  8. 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.

David J WisniewskiDepartment of Oncology and Diagnostic Sciences, School of Dentistry, University of Maryland, Baltimore, MD, USA.
Tao MaDepartment of Oncology and Diagnostic Sciences, School of Dentistry, University of Maryland, Baltimore, MD, USA.
Abraham SchneiderDepartment of Oncology and Diagnostic Sciences, School of Dentistry, University of Maryland, Baltimore, MD, USA.ORCID https://orcid.org/0000-0001-8046-9789
University of Maryland, Baltimore · US

Funding

Role of OCT-3 on metformin action in oral carcinogenesisR01DE023578 · NIDCR · UNIVERSITY OF MARYLAND BALTIMORE · PI SCHNEIDER, ABRAHAM · 2014 to 2018
$1.9M
NIDCR NIH HHS R01 DE023578
6 · The paper itself

Abstract

backgroundRecent studies point to the epidermal growth factor receptor (EGFR) as a critical mediator of type 2 diabetes mellitus (T2DM)-induced renal, cardiac, and ocular complications. T2DM is considered a systemic contributing factor in oral carcinogenesis. Similarly, increased EGFR gene copy number and protein expression strongly predict tumor progression. Yet, the impact of hyperglycemia on EGFR activity in oral potentially malignant disorders remains unclear. We recently reported that fatty acid synthase (FASN), a key de novo lipogenic enzyme, mediates EGFR activation in nicotine-treated oral dysplastic keratinocytes. While in non-malignant tissues FASN expression is extremely low, it is frequently upregulated in several cancers, including oral squamous cell carcinoma. The present study was carried out to investigate whether high glucose conditions trigger pro-oncogenic responses in oral dysplastic keratinocytes via FASN-mediated EGFR activation.

methodsCell viability and migration of oral dysplastic keratinocytes were evaluated when exposed to normal (5 mM) or high (20 mM) glucose conditions in the presence of FASN and EGFR inhibitors. Western blotting was also performed to assess changes in FASN protein expression and EGFR activation.

resultsOral dysplastic keratinocytes exposed to high glucose led to EGFR activation in a FASN-dependent manner. Likewise, high glucose significantly enhanced cell viability and migration in a FASN/EGFR-mediated fashion. Notably, EGFR inhibition by the anti-EGFR monoclonal antibody cetuximab significantly reduced the proliferation of FASN-overexpressing oral dysplastic keratinocytes.

conclusionThese novel findings suggest that FASN may act as a key targetable metabolic regulator of glucose-induced EGFR oncogenic signaling in oral potentially malignant disorders.

Indexed as

Carcinoma, Squamous CellDiabetes Mellitus, Type 2Mouth NeoplasmsCell Line, TumorErbB ReceptorsFatty Acid SynthasesGlucoseHumansKeratinocytesEGFR protein, humanErbB ReceptorsFatty Acid SynthasesGlucosediabetes mellitusEGFRFASNhyperglycemiaoral potentially malignant disorders

Identifiers

PMID34402100
PMCPMC8530891
OpenAlexW3194718686

What OpenQuestion 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 OpenQuestion graph.