Evidence map›Paper›PMID 31860169›Full record

Observational studyCancer medicine2020

LncRNA GMDS-AS1 inhibits lung adenocarcinoma development by regulating miR-96-5p/CYLD signaling.

Ming Zhao, Xiao-Feng Xin, Jian-Ya Zhang, Wei Dai, Tang-Feng Lv, Yong Song

Open access · goldAbstract readObservational Study
In one paragraph

Observational study in Cancer medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
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  9. Epigenetic inhibition of lncRNA GMDS-AS1 by methyltransferase ESET promoted cell viability and metastasis of hepatocellular carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
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  12. Review
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  18. MiR-96-5p Facilitates Lung Adenocarcinoma Cell Phenotypes by Inhibiting FHL1.Computational and mathematical methods in medicine · 2022
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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.

Ming ZhaoDepartment of Respiratory Medicine, Jinling Hospital, Second Military Medical University, Nanjing, China.ORCID 0000-0002-2871-1408
Xiao-Feng XinDepartment of Respiratory Medicine, Jinling Hospital, Second Military Medical University, Nanjing, China.
Jian-Ya ZhangDepartment of Respiratory Medicine, Jinling Hospital, Second Military Medical University, Nanjing, China.
Wei DaiDepartment of Respiratory Medicine, Jinling Hospital, Second Military Medical University, Nanjing, China.
Tang-Feng LvDepartment of Respiratory Medicine, Jinling Hospital, Second Military Medical University, Nanjing, China.
Yong SongDepartment of Respiratory Medicine, Jinling Hospital, Second Military Medical University, Nanjing, China.ORCID 0000-0003-4979-4131
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

According to the global cancer statistic, lung cancer is one of the most dangerous tumors, which poses a serious threat to human health. Exploration the mechanism of lung cancer and new targeted therapeutic measures is always the hot topic. Long noncoding RNA (lncRNA) is an important factor affecting the development of tumors. However, the research on the mechanism of lncRNA in the progress of lung cancer needs to be further expanded. In this study, we found that the expression of lncRNA GMDS-AS1 was significantly reduced in lung adenocarcinoma (LUAD) tissues and cells. Upregulated GMDS-AS1 can significantly inhibit the proliferation of LUAD cells and promote cell apoptosis in vitro and in vivo. The results indicate that GMDS-AS1 acts as a tumor suppressor gene to affect the development of LUAD. Further studies revealed that GMDS-AS1 is a target gene of miR-96-5p, and GMDS-AS1 regulates proliferation and apoptosis of LUAD cells in association with miR-96-5p. In addition, we also confirmed that CYLD lysine 63 deubiquitinase (CYLD) is also a target gene of miR-96-5p. Through various validations, we confirmed that GMDS-AS1 can act as a ceRNA to upregulate the expression of CYLD by sponging miR-96-5p. Moreover, the intervention of GMDS-AS1/miR-96-5p/CYLD network can regulate the proliferation and apoptosis of LUAD cells. In this study, we revealed that the GMDS-AS1/miR-96-5p/CYLD network based on ceRNA mechanism plays an important role in the development of LUAD and provides a new direction and theoretical basis for targeted therapy of LUAD.

Indexed as

A549 CellsAdenocarcinoma of LungApoptosisCell Line, TumorCell ProliferationDeubiquitinating Enzyme CYLDFemaleGene Expression Regulation, NeoplasticHumansLungLung NeoplasmsMaleMicroRNAsMiddle AgedRNA, Long NoncodingSignal TransductionCYLD protein, humanDeubiquitinating Enzyme CYLDMicroRNAsMIRN96 microRNA, humanRNA, Long NoncodingCYLDlncRNA GMDS-AS1lung adenocarcinomamiR-96-5p

Identifiers

PMID31860169
PMCPMC6997056
OpenAlexW2994769746

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LicenceCC BY
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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.