Evidence map›Paper›PMID 26336823›Full record

ArticleOncotarget2015

Inactivation of M2 AChR/NF-κB signaling axis reverses epithelial-mesenchymal transition (EMT) and suppresses migration and invasion in non-small cell lung cancer (NSCLC).

Qingnan Zhao, Jinnan Yue, Chun Zhang, Xiajing Gu, Hongzhuan Chen, Lu Xu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-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

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. The Role of the Nervous System in Lung Disease.Current neurology and neuroscience reports · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Reposition of the anti-inflammatory drug diacerein in anSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022
    Article
  11. Review
  12. Role of the parasympathetic nervous system in cancer initiation and progression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Review
  13. Article
  14. Observational
  15. Review
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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 1 institution in 1 country.

Qingnan ZhaoDepartment of Pharmacology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jinnan YueDepartment of Pharmacology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chun ZhangDepartment of Pharmacology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiajing GuDepartment of Pharmacology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hongzhuan ChenDepartment of Pharmacology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Lu XuDepartment of Pharmacology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-neuronal cholinergic system is involved in lung physiology and lung cancer. However, the biochemical events downstream acetylcholine (ACh) receptor activation leading to carcinogenesis and tumor progression are not fully understood. Our previous work has shown that non-neuronal ACh acts as an autoparacrine growth factor to stimulate cell proliferation and promote epithelial-mesenchymal transition (EMT) in non-small cell lung cancer (NSCLC) via activation of M2 muscarinic receptor (M2R). The aim of the present study was to delineate the underlying mechanisms linking M2R and lung tumor progression, which may provide potential therapeutic targets to delay lung cancer progression. Inhibition of M2R by antagonist or siRNA suppresses NSCLC cell migratory and invasive capacities, reverses EMT and simultaneously inactivates PI3K/Akt, MAPK ERK and NF-κB p65. On the other hand, M2R activation stimulates NSCLC migration and invasion and promotes EMT via NF-κB p65 activation. Moreover, NF-κB p65 activation induced by M2R activation was partially inhibited by either Akt or ERK inhibitor. Taken together, these results demonstrated for the first time that NF-κB p65 activation is essential in NSCLC progression associated with non-neuronal cholinergic system. Our data suggest that M2R/ERK/Akt/NF-κB axis could be a potential target for NSCLC treatment.

Indexed as

Cell MovementEpithelial-Mesenchymal TransitionSignal TransductionCarcinoma, Non-Small-Cell LungCell Line, TumorExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, NeoplasticHumansLung NeoplasmsMuscarinic AntagonistsNeoplasm InvasivenessPhosphatidylinositol 3-KinaseProtein Kinase InhibitorsProto-Oncogene Proteins c-aktReceptor, Muscarinic M2RNA InterferenceCHRM2 protein, humanExtracellular Signal-Regulated MAP KinasesMuscarinic AntagonistsPhosphatidylinositol 3-KinaseProtein Kinase InhibitorsProto-Oncogene Proteins c-aktReceptor, Muscarinic M2RELA protein, humanTranscription Factor RelAEMTM2 muscarinic receptorNF-κBnon-neuronal cholinergic systemNSCLC

Identifiers

PMID26336823
PMCPMC4745730
OpenAlexW1799614271

What OpenQuestion holds

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Read underepoch 390

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.