Evidence map›Paper›PMID 26919111›Full record

ArticleOncotarget2016

MACC1 mediates acetylcholine-induced invasion and migration by human gastric cancer cells.

Ting Yang, Wanming He, Fei Cui, Jianling Xia, Rui Zhou, Zhenzhen Wu, Yang Zhao, Min Shi

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
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  10. Article
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  13. 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
  14. Article
  15. Review
  16. Review
  17. Role of the brain-gut axis in gastrointestinal cancer.World journal of clinical cases · 2019
    Review
  18. Review
  19. Article
  20. Role of the nervous system in cancer metastasis.Journal of experimental & clinical cancer research : CR · 2018
    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

8 authors at 2 institutions in 1 country.

Ting YangDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Wanming HeDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Fei CuiDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jianling XiaDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Rui ZhouDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Zhenzhen WuDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yang ZhaoDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Min ShiDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Nanfang Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The neurotransmitter acetylcholine (ACh) promotes the growth and metastasis of several cancers via its M3 muscarinic receptor (M3R). Metastasis-associated in colon cancer-1 (MACC1) is an oncogene that is overexpressed in gastric cancer (GC) and plays an important role in GC progression, though it is unclear how MACC1 activity is regulated in GC. In this study, we demonstrated that ACh acts via M3Rs to promote GC cell invasion and migration as well as expression of several markers of epithelial-mesenchymal transition (EMT). The M3R antagonist darifenacin inhibited GC cell activity in both the presence and absence of exogenous ACh, suggesting GC cells secrete endogenous ACh, which then acts in an autocrine fashion to promote GC cell migration/invasion. ACh up-regulated MACC1 in GC cells, and MACC1 knockdown using siRNA attenuated the effects of ACh on GC cells. AMP-activated protein kinase (AMPK) served as an intermediate signal between ACh and MACC1. These findings suggest that ACh acts via a M3R/AMPK/MACC1 signaling pathway to promote GC cell invasion/migration, which provides insight into the mechanisms underlying GC growth and metastasis and may shed light on new targets for GC treatment.

Indexed as

AcetylcholineAMP-Activated Protein KinasesBenzofuransCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMuscarinic AntagonistsNeoplasm InvasivenessPyrrolidinesReceptor, Muscarinic M3RNA InterferenceRNA, Small InterferingSignal TransductionAcetylcholineAMP-Activated Protein KinasesBenzofuransdarifenacinMACC1 protein, humanMuscarinic AntagonistsPyrrolidinesReceptor, Muscarinic M3RNA, Small InterferingTrans-ActivatorsTranscription Factorsacetylcholinegastric cancerinvasionMACC1migration

Identifiers

PMID26919111
PMCPMC4951273
OpenAlexW2293682234

What OpenQuestion holds

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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.