Evidence map›Paper›PMID 32001831›Full record

ArticleBritish journal of cancer2020

Nicotine exposure potentiates lung tumorigenesis by perturbing cellular surveillance.

Qiang Zhang, Suthakar Ganapathy, Hava Avraham, Takashi Nishioka, Changyan Chen

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
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  7. Article
  8. Multifaceted roles of mitochondria in asthma.Cell biology and toxicology · 2024
    Review
  9. Cell signaling and epigenetic regulation of nicotine-induced carcinogenesis.Environmental pollution (Barking, Essex : 1987) · 2024
    Review
  10. Nicotinic receptors in airway disease.American journal of physiology. Lung cellular and molecular physiology · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. GRP78 in lung cancer.Journal of translational medicine · 2021
    Review
  16. α9-Containing Nicotinic Receptors in Cancer.Frontiers in cellular neuroscience · 2021
    Review
  17. Article
  18. Article
  19. Protective Effects ofIn vivo (Athens, Greece)
    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

5 authors at 3 institutions in 3 countries.

Qiang Zhang *The First Affiliated Hospital of Nanchang University, Nanchang, P.R. China.
Suthakar Ganapathy *Center for Drug Development, Northeastern University, Boston, MA, USA.
Hava AvrahamCenter for Drug Development, Northeastern University, Boston, MA, USA.
Takashi NishiokaTohoku University Graduate School of Dentistry, Sendai, Japan.
Changyan ChenCenter for Drug Development, Northeastern University, Boston, MA, USA. c.changyan@northeastern.edu.
Northeastern University · USFirst Affiliated Hospital of Nanchang University · CNTohoku University · JP

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81260169National Natural Science Foundation of China (National Science Foundation of China) 81560189
6 · The paper itself

Abstract

backgroundNicotine is a major tobacco component and found at circulating concentrations in smokers' bloodstreams. Although considered a non-carcinogenic substance, nicotine rapidly defuses to tissues after being inhaled, inviting effects on cellular physiology, particularly in the lung. Widespread increased use of nicotine-based e-cigarettes, especially in younger adults, creates an urgent need for improved understanding of nicotine's potential to impact human health.

methodsBiological and biochemistry methods were used to interrogate the potential for nicotine to weaken the genetic integrity of murine and human-lung epithelial cells.

resultsWe demonstrate that nicotine potentiates the growth of the lung epithelial cells in a dose-response fashion. Nicotine elicits an acute increase in reactive oxygen species (ROS), which persists at moderately high levels throughout the duration of nicotine exposure. The aberrant increases in ROS appear to induce ER stress and UPR activation, as reflected by BIP upregulation and PERK phosphorylation. Furthermore, prolonged nicotine exposure interferes with p53 function triggered by sodium arsenite. Unless p53 is suppressed, persistent nicotine exposure does not induce colony formation by lung epithelial cells in soft agar.

conclusionThe data suggest that nicotine treatment, by perturbing intracellular redox state and altering p53 function, can create a pro-tumorigenic environment in lung epithelium. The results suggest caution in using nicotine replacement therapies and e-cigarettes.

Indexed as

AnimalsCarcinogenesisEpithelial CellsHumansLung NeoplasmsMiceNicotineNicotine

Identifiers

PMID32001831
PMCPMC7078213
OpenAlexW3003966541

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.