Evidence map›Paper›PMID 25520033›Full record

ArticleScientific reports2014

Biological and clinical significance of epigenetic silencing of MARVELD1 gene in lung cancer.

Ming Shi, Shan Wang, Yuanfei Yao, Yiqun Li, Hao Zhang, Fang Han, Huan Nie, Jie Su, Zeyu Wang, Lei Yue and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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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

12 authors at 2 institutions in 1 country.

Ming ShiSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Shan WangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Yuanfei YaoSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Yiqun LiSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Hao ZhangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Fang HanSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Huan NieSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Jie SuSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Zeyu WangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Lei YueSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Jingyan CaoDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Yu LiSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Harbin Institute of Technology · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic silence in cancer frequently altered signal-transduction pathways during the early stages of tumor development. Recent progress in the field of cancer epigenetics has led to new opportunities for diagnosis and treatment of cancer. We previously demonstrated that novel identified nuclear factor MARVELD1 was widely expressed in human tissues, but down-regulated by promoter methylation in multiple cancers. This study was carried out to determine the biological and clinical significance of MARVELD1 gene silencing in lung cancer. Here, we found the reduced MARVELD1 expression significantly correlated with diagnostic histopathology and malignant degree of lung cancers. DNA hypermethylation and histone deacetylation synergistically inactivated MARVELD1 gene in lung cancer cells. Moreover, MARVELD1 modulated the efficiency of nonsense-mediated mRNA decay (NMD) through interaction with NMD core factor SMG1. The decreased MARVELD1 level in lung cancer reduces NMD efficiency through diminishing the association between NMD complex component UPF1/SMG1 and premature termination codons containing mRNA (PTC-mRNA). The results suggested that MARVELD1 silencing is an appealing diagnostic biomarker for lung cancer and epigenetic silencing of MARVELD1 gene links with the regulatory mechanism of NMD pathway in lung cancer, which may be required for tumorigenesis.

Indexed as

Biomarkers, TumorCell Line, TumorCodon, NonsenseDNA MethylationEpigenesis, GeneticGene Expression ProfilingGene SilencingHistonesHumansLung NeoplasmsMembrane ProteinsMicrotubule-Associated ProteinsNonsense Mediated mRNA DecaySignal TransductionBiomarkers, TumorCodon, NonsenseHistonesMARVELD1 protein, humanMembrane ProteinsMicrotubule-Associated Proteins

Identifiers

PMID25520033
PMCPMC4269892
OpenAlexW2005716799

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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.