Evidence map›Paper›PMID 29966661›Full record

ArticleExperimental cell research2018

Nicotine induces oral dysplastic keratinocyte migration via fatty acid synthase-dependent epidermal growth factor receptor activation.

David J Wisniewski, Tao Ma, Abraham Schneider

Open access · greenAbstract read
In one paragraph

Article in Experimental cell research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

11 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. E-Cigarette effects on oral health: A molecular perspective.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2025
    Review
  3. E-cigarette: a safe tool or a risk factor for oral cancer? A systematic review.Journal of clinical and experimental dentistry · 2025
    Review
  4. Review
  5. 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
  6. Article
  7. Review
  8. Fatty acid synthase mediates high glucose-induced EGFR activation in oral dysplastic keratinocytes.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2021
    Article
  9. Review
  10. Nicotine mediated epithelial modulations: AnJournal of oral biology and craniofacial research
    Article
  11. 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; Marlene and Stewart Greenebaum Comprehensive Cancer Center, Program in Oncology, School of Medicine, University of Maryland, Baltimore, MD, USA. Electronic address: schneider66@umaryland.edu.
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

Despite advances in diagnostic and therapeutic management, oral squamous cell carcinoma (OSCC) patient survival rates have remained relatively unchanged. Thus, identifying early triggers of malignant progression is critical to prevent OSCC development. Traditionally, OSCC initiation is elicited by the frequent and direct exposure to multiple tobacco-derived carcinogens, and not by the nicotine contained in tobacco products. However, other nicotine-containing products, especially the increasingly popular electronic cigarettes (e-cigs), have unknown effects on the progression of undiagnosed tobacco-induced oral premalignant lesions, specifically in regard to the effects of nicotine. Overexpression of fatty acid synthase (FASN), a key hepatic de novo lipogenic enzyme, is linked to poor OSCC patient survival. Nicotine upregulates hepatic FASN, but whether this response occurs in oral dysplastic keratinocytes is unknown. We hypothesized that in oral dysplastic keratinocytes, nicotine triggers a migratory phenotype through FASN-dependent epidermal growth factor receptor (EGFR) activation, a common pro-oncogenic event supporting oral carcinogenesis. We report that in oral dysplastic cells, nicotine markedly upregulates FASN leading to FASN-dependent EGFR activation and increased cell migration. These results raise potential concerns about e-cig safety, especially when used by former tobacco smokers with occult oral premalignant lesions where nicotine could trigger oncogenic signals commonly associated with malignant progression.

Indexed as

CarcinogenesisCarcinoma, Squamous CellCell Line, TumorCell MovementElectronic Nicotine Delivery SystemsErbB ReceptorsFatty Acid SynthasesHumansKeratinocytesMouth NeoplasmsNicotinePrecancerous ConditionsUp-RegulationErbB ReceptorsFatty Acid SynthasesNicotineCell migrationEGFRFASNNicotineOral cancerOral premalignant lesions

Identifiers

PMID29966661
PMCPMC6108942
OpenAlexW2810877903

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.