Evidence map›Paper›PMID 28447759›Full record

ArticleMolecular medicine reports2017

miR-181a modulates proliferation, migration and autophagy in AGS gastric cancer cells and downregulates MTMR3.

Yong Lin, Jing Zhao, Hong Wang, Jie Cao, Yuqiang Nie

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

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  12. Virus, Exosome, and MicroRNA: New Insights into Autophagy.Advances in experimental medicine and biology · 2022
    Article
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  20. The Role of Autophagy in Gastric Cancer Chemoresistance: Friend or Foe?Frontiers in cell and developmental biology · 2020
    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

5 authors at 1 institution in 1 country.

Yong LinDepartment of Gastroenterology, Guangzhou Digestive Disease Center, Guangzhou Key Laboratory of Digestive Disease, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China.
Jing ZhaoSchool of Public Health, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China.
Hong WangDepartment of Gastroenterology, Guangzhou Digestive Disease Center, Guangzhou Key Laboratory of Digestive Disease, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China.
Jie CaoDepartment of General Surgery, Guangzhou Digestive Disease Center, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China.
Yuqiang NieDepartment of Gastroenterology, Guangzhou Digestive Disease Center, Guangzhou Key Laboratory of Digestive Disease, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China.
Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRs) have emerged as crucial regulators of tumorigenesis by regulating post-transcriptional gene expression. miR-181a was previously demonstrated to be overexpressed in human gastric cancer tissues and cell lines, whereas MTMR3 was underexpressed. The MTMR3 gene was identified as a direct target of miR-181a. However, its functional role in gastric cancer remains to be established. In the present study, miR‑181a was demonstrated to inhibit MTMR3 expression in AGS cells. Ectopic expression of miR‑181a mimics or introduction of MTMR3 small interfering RNA resulted in an increase in cell proliferation, colony formation, migration, invasion, as well as suppression of apoptosis. Further investigation in the present study indicated that overexpression of miR‑181a, or depletion of MTMR3, attenuated starvation‑induced autophagy in AGS cells. In addition, inhibition of endogenous miR‑181a led to stimulation of autophagic activity. Collectively, these data suggest that miR‑181a is a novel regulator of gastric cancer progression and autophagy, and miR-181a modulation may be a potential strategy for the development of miRNA‑based therapeutics for gastric cancer.

Indexed as

AutophagyCell MovementCell ProliferationCell Line, TumorHumansMicroRNAsRNA, NeoplasmStomach NeoplasmsMicroRNAsMIrn181 microRNA, humanRNA, Neoplasm

Identifiers

PMID28447759
PMCPMC5428200
OpenAlexW2592146022

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.