Evidence map›Paper›PMID 22942701›Full record

ArticleInternational journal of molecular sciences2012

Genome-wide analysis of DNA methylation and expression of microRNAs in breast cancer cells.

Sumiyo Morita, Ryou-U Takahashi, Riu Yamashita, Atsushi Toyoda, Takuro Horii, Mika Kimura, Asao Fujiyama, Kenta Nakai, Shoji Tajima, Ryo Matoba and 2 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2012. 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
2.8field-weighted citation impact, top 9% 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, 38 citations in OpenAlex.

  1. Review
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  4. Impact of Natural OccurringInternational journal of molecular sciences · 2020
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  10. Noncoding RNAs in breast cancer.Briefings in functional genomics · 2016
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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 6 institutions in 1 country.

Sumiyo MoritaLaboratory of Genome Science, Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University, Gunma 371-8512, Japan.
Ryou-U TakahashiDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute, 5-1-1, Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.
Riu YamashitaDepartment of Integrative Genomics, Medical Megabank Organization, Tohoku University, 6-3-09, aza Aoba, Aramaki, Aobaku, Sendai 980-8579, Japan.
Atsushi ToyodaCenter for Genetic Resource Information, National Institute of Genetics, Shizuoka 411-8540, Japan.
Takuro HoriiLaboratory of Genome Science, Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University, Gunma 371-8512, Japan.
Mika KimuraLaboratory of Genome Science, Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University, Gunma 371-8512, Japan.
Asao FujiyamaCenter for Genetic Resource Information, National Institute of Genetics, Shizuoka 411-8540, Japan.
Kenta NakaiHuman Genome Center, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
Shoji TajimaLaboratory of Epigenetics, Institute for Protein Research, Osaka University, 3-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Ryo MatobaDNA Chip Research Inc., 1-1-43 Suehirocho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan.
Takahiro OchiyaDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute, 5-1-1, Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.
Izuho HatadaLaboratory of Genome Science, Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University, Gunma 371-8512, Japan.
Gunma University · JPNational Institute of Genetics · JPDNA Chip Research (Japan) · JPOsaka University · JPTohoku Medical Megabank Organization · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA methylation of promoters is linked to transcriptional silencing of protein-coding genes, and its alteration plays important roles in cancer formation. For example, hypermethylation of tumor suppressor genes has been seen in some cancers. Alteration of methylation in the promoters of microRNAs (miRNAs) has also been linked to transcriptional changes in cancers; however, no systematic studies of methylation and transcription of miRNAs have been reported. In the present study, to clarify the relation between DNA methylation and transcription of miRNAs, next-generation sequencing and microarrays were used to analyze the methylation and expression of miRNAs, protein-coding genes, other non-coding RNAs (ncRNAs), and pseudogenes in the human breast cancer cell lines MCF7 and the adriamycin (ADR) resistant cell line MCF7/ADR. DNA methylation in the proximal promoter of miRNAs is tightly linked to transcriptional silencing, as it is with protein-coding genes. In protein-coding genes, highly expressed genes have CpG-rich proximal promoters whereas weakly expressed genes do not. This is only rarely observed in other gene categories, including miRNAs. The present study highlights the epigenetic similarities and differences between miRNA and protein-coding genes.

Indexed as

DNA MethylationBreast NeoplasmsCpG IslandsFemaleGene Expression Regulation, NeoplasticGenome, HumanHumansMCF-7 CellsMicroRNAsSequence Analysis, DNATranscription Initiation SiteTranscriptomeMicroRNAscancerDNA methylationmicroRNA

Identifiers

PMID22942701
PMCPMC3430232
OpenAlexW1984121949

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.