Evidence map›Paper›PMID 25272045›Full record

ArticlePloS one2014

MiR-410 is overexpressed in liver and colorectal tumors and enhances tumor cell growth by silencing FHL1 via a direct/indirect mechanism.

Yu Wang, Jie Fu, Mengmeng Jiang, Xiaoai Zhang, Long Cheng, Xiaojie Xu, Zhongyi Fan, Jing Zhang, Qinong Ye, Haifeng Song

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.1field-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

33 citing papers in PubMed, 55 citations in OpenAlex.

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  10. MiR-96-5p Facilitates Lung Adenocarcinoma Cell Phenotypes by Inhibiting FHL1.Computational and mathematical methods in medicine · 2022
    Article
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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

10 authors at 3 institutions in 1 country.

Yu WangDepartment of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing, China; SDU School of Life Science, Jinan, China.
Jie FuDepartment of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing, China.
Mengmeng JiangDepartment of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing, China.
Xiaoai ZhangState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, China.
Long ChengDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing, China.
Xiaojie XuDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing, China.
Zhongyi FanDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing, China.
Jing ZhangDepartment of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing, China.
Qinong YeDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing, China.
Haifeng SongDepartment of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing, China.
Beijing Radiation Center · CNBeijing VDJBio (China) · CNInstitute of Microbiology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FHL1 is an important tumor-suppressor that is downregulated in multiple tumors by unknown mechanisms. We demonstrated that miR-410 specifically targets the 3'UTR of FHL1. Furthermore, using DNA bisulfite modification and sequencing experiments, we demonstrated that the FHL1 promoter is hypermethylated in cancer cells. FHL1 methylation is increased upon miR-410 expression, suggesting that the regulation of FHL1 by miR-410 occurs by a dual mechanism. Using chromatin immunoprecipitation assays, we observed that miR-410 overexpression results in the increased binding of DNMT3A at the FHL1 promoter, which could explain how miR-410 regulates FHL1 methylation. Importantly, in vitro and in vivo results suggest that miR-410 may have oncogenic properties. Furthermore, both miR-410 and DNMT3A are upregulated in clinical human liver and colorectal tumors cancers. Our results suggest that miR-410 may function as an oncomiR and are consistent with its key function in regulating FHL1 in certain digestive system cancers.

Indexed as

Gene Silencing3' Untranslated RegionsAnimalsCell Line, TumorColorectal NeoplasmsDisease Models, AnimalDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3AGene Expression Regulation, NeoplasticHeterograftsHumansIntracellular Signaling Peptides and ProteinsLIM Domain ProteinsLiver NeoplasmsMaleMicroRNAs3' Untranslated RegionsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, humanFHL1 protein, humanIntracellular Signaling Peptides and ProteinsLIM Domain ProteinsMicroRNAsMIRN410 microRNA, humanMuscle Proteins

Identifiers

PMID25272045
PMCPMC4182719
OpenAlexW2030925636

What OpenQuestion holds

Textmetadata
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.