Evidence map›Paper›PMID 29843634›Full record

ArticleBMC cancer2018

GMDS knockdown impairs cell proliferation and survival in human lung adenocarcinoma.

Xing Wei, Kun Zhang, Haifeng Qin, Jinlong Zhu, Qiaoxi Qin, Yang Yu, Hong Wang

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Xing WeiOutpatient Department, Southern Theatre Command of People's Liberation Army, Guangzhou, 510080, Guangdong, China.
Kun ZhangDepartment of Lung Cancer, The Affiliated Hospital of Military Medical Sciences, The 307th Hospital of Chinese People's Liberation Army, Beijing, 100071, China.
Haifeng QinDepartment of Lung Cancer, The Affiliated Hospital of Military Medical Sciences, The 307th Hospital of Chinese People's Liberation Army, Beijing, 100071, China.
Jinlong ZhuDepartment of Lung Cancer, The Affiliated Hospital of Military Medical Sciences, The 307th Hospital of Chinese People's Liberation Army, Beijing, 100071, China.
Qiaoxi QinDepartment of Lung Cancer, The Affiliated Hospital of Military Medical Sciences, The 307th Hospital of Chinese People's Liberation Army, Beijing, 100071, China.
Yang YuDepartment of Lung Cancer, The Affiliated Hospital of Military Medical Sciences, The 307th Hospital of Chinese People's Liberation Army, Beijing, 100071, China.
Hong WangDepartment of Lung Cancer, The Affiliated Hospital of Military Medical Sciences, The 307th Hospital of Chinese People's Liberation Army, Beijing, 100071, China. 18511244323@163.com.ORCID http://orcid.org/0000-0001-5276-9821
307th Hospital of Chinese People’s Liberation Army · CNThird Affiliated Hospital of Southern Medical University · CN

Funding

National Natural Science Foundation of China 81572266
6 · The paper itself

Abstract

backgroundLung adenocarcinoma is the most common type of lung cancer and one of the most lethal and prevalent cancers. Aberrant glycosylation was common and essential in tumorigenesis, with fucosylation as one of the most common types disrupted in cancers. However, it is still unknown whether genes involved in fucosylation are important for lung adenocarcinoma development and process.

methodsGMDS is involved in cellular fucosylation. Here we examined GMDS expression level at both mRNA and protein level in lung adenocarcinoma. The impact of GMDS knockdown on lung adenocarcinoma in vitro and in vivo was investigated. Transcriptome changes with GMDS knockdown in lung adenocarcinoma cells were also examined to provide insights into related molecular mechanisms.

resultsGMDS expression is significantly upregulated in lung adenocarcinoma at both mRNA and protein levels. Lentivirus-mediated shRNA strategy inhibited GMDS expression efficiently in human lung adenocarcinoma cells A549 and H1299, and GMDS knockdown impaired cell proliferation, colony formation ability, induced cell cycle arrest, and apoptosis in both cell lines. Furthermore, GMDS knockdown inhibited tumorigenesis in a xenograft mice model of lung adenocarcinoma. Microarray analysis explored the GMDS-mediated molecular network and revealed that the CASP8-CDKN1A axis might be critical for lung adenocarcinoma development.

conclusionsThese findings suggest that GMDS upregulation is critical for cell proliferation and survival in human lung adenocarcinoma and might serve as a potential biomarker for lung adenocarcinoma diagnosis and treatment.

Indexed as

Gene Expression Regulation, NeoplasticA549 CellsAdenocarcinoma of LungAgedAnimalsApoptosisBiomarkers, TumorCarcinogenesisCell ProliferationCell SurvivalDisease ProgressionFemaleGene Expression ProfilingGene Knockdown TechniquesGlycosylationHumansBiomarkers, TumorGDPmannose 4,6-dehydrataseGMDS protein, humanHydro-LyasesRNA, MessengerRNA, Small InterferingCell proliferationGMDSLung adenocarcinomaMolecular networkSurvivalTumorigenesis

Identifiers

PMID29843634
PMCPMC5975429
OpenAlexW2806768597

What OpenQuestion holds

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LicenceCC BY
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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.