Evidence map›Paper›PMID 23300583›Full record

ArticlePloS one2012

Nicotine promotes acquisition of stem cell and epithelial-to-mesenchymal properties in head and neck squamous cell carcinoma.

Michael Andrew Yu, Alan Kiang, Jessica Wang-Rodriguez, Elham Rahimy, Martin Haas, Vicky Yu, Lesley G Ellies, Jing Chen, Jian-Bing Fan, Kevin T Brumund and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

36 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Cell signaling and epigenetic regulation of nicotine-induced carcinogenesis.Environmental pollution (Barking, Essex : 1987) · 2024
    Review
  6. Review
  7. Effect of Nicotine on Immune System Function.Advanced pharmaceutical bulletin · 2023
    Review
  8. Review
  9. Review
  10. Article
  11. Epimutational effects of electronic cigarettes.Environmental science and pollution research international · 2021
    Review
  12. Article
  13. Review
  14. Article
  15. Environmental chemicals, breast cancer progression and drug resistance.Environmental health : a global access science source · 2020
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Environmental exposures, stem cells, and cancer.Pharmacology & therapeutics · 2019
    Review
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

12 authors at 2 institutions in 1 country.

Michael Andrew YuDivision of Otolaryngology-Head and Neck Surgery, Department of Surgery, University of California San Diego, La Jolla, CA, USA.
Alan Kiang
Jessica Wang-Rodriguez
Elham Rahimy
Martin Haas
Vicky Yu
Lesley G Ellies
Jing Chen
Jian-Bing Fan
Kevin T Brumund
Robert A Weisman
Weg M Ongkeko
University of California, San Diego · USIllumina (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ability of nicotine to enhance the malignancy of cancer cells is known; however, the possibility that nicotine could regulate a cancer stem cell phenotype remains to be well-established. In this study we sought to determine whether long-term exposure to nicotine could promote cancer stem cell-like properties in two head and neck squamous cell carcinoma cell lines, UMSCC-10B and HN-1. Nicotine treatment induced epithelial-to-mesenchymal transition (EMT) in both cell lines by repressing E-cadherin expression, and led to the induction of stem cell markers Oct-4, Nanog, CD44 and BMI-1, which was reversed upon ectopic re-expression of E-cadherin. Nicotine-treated cells formed spheres at a higher efficiency than non-treated cells, formed larger tumors when injected into mice, and formed tumors with 4-fold greater efficiency compared to control cells when injected at limiting doses. Consistent with previous literature, nicotine-treated cells demonstrated a greater capacity for survival and also a higher tendency to invade. Comparison of microRNA profiles between nicotine and control cells revealed the upregulation of miR-9, a repressor of E-cadherin, and the downregulation of miR-101, a repressor of EZH2. Taken together, these results suggest that nicotine may play a critical role in the development of tobacco-induced cancers by regulating cancer stem cell characteristics, and that these effects are likely mediated through EMT-promoting, microRNA-mediated pathways. Further characterization of such pathways remains a promising avenue for the understanding and treatment of tobacco-related cancers.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsApoptosisBiomarkers, TumorBlotting, WesternCadherinsCarcinoma, Squamous CellCell MovementCell ProliferationCells, CulturedFluorescent Antibody TechniqueGene Expression ProfilingHead and Neck NeoplasmsHumansImmunoenzyme TechniquesMiceBiomarkers, TumorCadherinsMicroRNAsNicotineNicotinic AgonistsRNA, Messenger

Identifiers

PMID23300583
PMCPMC3530520
OpenAlexW2131666116

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.