Evidence map›Paper›PMID 31930655›Full record

ArticleJournal of cellular and molecular medicine2020

α5-nAChR contributes to epithelial-mesenchymal transition and metastasis by regulating Jab1/Csn5 signalling in lung cancer.

Xiaowei Chen, Yanfei Jia, Yujie Zhang, Dajie Zhou, Haiji Sun, Xiaoli Ma

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Smoking-Induced STC2Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Cell signaling and epigenetic regulation of nicotine-induced carcinogenesis.Environmental pollution (Barking, Essex : 1987) · 2024
    Review
  15. Nicotinic receptors in airway disease.American journal of physiology. Lung cellular and molecular physiology · 2024
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

6 authors at 3 institutions in 1 country.

Xiaowei ChenCentral Laboratory, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Yanfei JiaCentral Laboratory, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Yujie ZhangWeifang Medical University, Weifang, China.
Dajie ZhouWeifang Medical University, Weifang, China.
Haiji SunKey Laboratory of Animal Resistance Biology of Shandong Province, School of Life Science, Shandong Normal University, Jinan, China.
Xiaoli MaCentral Laboratory, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.ORCID 0000-0003-0279-8354
Shandong University · CNWeifang Medical University · CNShandong Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have showed that α5 nicotinic acetylcholine receptor (α5-nAChR) is closely associated with nicotine-related lung cancer. Our previous studies also demonstrated that α5-nAChR mediates nicotine-induced lung carcinogenesis. However, the mechanism by which α5-nAChR functions in lung carcinogenesis remains to be elucidated. Jab1/Csn5 is a key regulatory factor in smoking-induced lung cancer. In this study, we explored the underlying mechanisms linking the α5-nAChR-Jab1/Csn5 axis with lung cancer epithelial-mesenchymal transition (EMT) and metastasis, which may provide potential therapeutic targets for future lung cancer treatments. Our results demonstrated that the expression of α5-nAChR was correlated with the expression of Jab1/Csn5 in lung cancer tissues and lung cancer cells. α5-nAChR expression is associated with Jab1/Csn5 expression in lung tumour xenografts in mice. In vitro, the expression of α5-nAChR mediated Stat3 and Jab1/Csn5 expression, significantly regulating the expression of the EMT markers, N-cadherin and Vimentin. In addition, the down-regulation of α5-nAChR or/and Stat3 reduced Jab1/Csn5 expression, while the silencing of α5-nAChR or Jab1/Csn5 inhibited the migration and invasion of NSCLC cells. Mechanistically, α5-nAChR contributes to EMT and metastasis by regulating Stat3-Jab1/Csn5 signalling in NSCLC, suggesting that α5-nAChR may be a potential target in NSCLC diagnosis and immunotherapy.

Indexed as

A549 CellsAnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCOP9 Signalosome ComplexDown-RegulationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsLung NeoplasmsMaleMiceMice, Inbred BALB CCOP9 Signalosome ComplexCOPS5 protein, humanIntracellular Signaling Peptides and ProteinsPeptide HydrolasesReceptors, Nicotinicepithelial-mesenchymal transitionJab1/Csn5non-small-cell lung cancerα5-nicotinic acetylcholine receptor

Identifiers

PMID31930655
PMCPMC7028847
OpenAlexW3000435944

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Registered trials

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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.