Evidence map›Paper›PMID 25673149›Full record

ArticleScientific reports2015

The miR-199a/Brm/EGR1 axis is a determinant of anchorage-independent growth in epithelial tumor cell lines.

Kazuyoshi Kobayashi, Kouhei Sakurai, Hiroaki Hiramatsu, Ken-ichi Inada, Kazuya Shiogama, Shinya Nakamura, Fumiko Suemasa, Kyosuke Kobayashi, Seiya Imoto, Takeshi Haraguchi and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 14 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

14 authors at 2 institutions in 1 country.

Kazuyoshi KobayashiDivision of Host-Parasite Interaction, Department of Microbiology and Immunology, University of Tokyo, Tokyo, Japan.
Kouhei SakuraiDivision of Host-Parasite Interaction, Department of Microbiology and Immunology, University of Tokyo, Tokyo, Japan.
Hiroaki HiramatsuDivision of Host-Parasite Interaction, Department of Microbiology and Immunology, University of Tokyo, Tokyo, Japan.
Ken-ichi InadaFirst Department of Pathology, Faculty of Medicine, Fujita Health University, Aichi, Japan.
Kazuya ShiogamaFirst Department of Pathology, Faculty of Medicine, Fujita Health University, Aichi, Japan.
Shinya NakamuraDivision of Host-Parasite Interaction, Department of Microbiology and Immunology, University of Tokyo, Tokyo, Japan.
Fumiko SuemasaDivision of Host-Parasite Interaction, Department of Microbiology and Immunology, University of Tokyo, Tokyo, Japan.
Kyosuke KobayashiDivision of Host-Parasite Interaction, Department of Microbiology and Immunology, University of Tokyo, Tokyo, Japan.
Seiya ImotoLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Takeshi HaraguchiDivision of Host-Parasite Interaction, Department of Microbiology and Immunology, University of Tokyo, Tokyo, Japan.
Hiroaki ItoDivision of Host-Parasite Interaction, Department of Microbiology and Immunology, University of Tokyo, Tokyo, Japan.
Aya IshizakaDivision of Host-Parasite Interaction, Department of Microbiology and Immunology, University of Tokyo, Tokyo, Japan.
Yutaka TsutsumiFirst Department of Pathology, Faculty of Medicine, Fujita Health University, Aichi, Japan.
Hideo IbaDivision of Host-Parasite Interaction, Department of Microbiology and Immunology, University of Tokyo, Tokyo, Japan.
The University of Tokyo · JPFujita Health University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In epithelial cells, miRNA-199a-5p/-3p and Brm, a catalytic subunit of the SWI/SNF complex were previously shown to form a double-negative feedback loop through EGR1, by which human cancer cell lines tend to fall into either of the steady states, types 1 [miR-199a(-)/Brm(+)/EGR1(-)] and 2 [miR-199a(+)/Brm (-)/EGR1(+)]. We show here, that type 2 cells, unlike type 1, failed to form colonies in soft agar, and that CD44, MET, CAV1 and CAV2 (miR-199a targets), all of which function as plasma membrane sensors and can co-localize in caveolae, are expressed specifically in type 1 cells. Single knockdown of any of them suppressed anchorage-independent growth of type 1 cells, indicating that the miR-199a/Brm/EGR1 axis is a determinant of anchorage-independent growth. Importantly, two coherent feedforward loops are integrated into this axis, supporting the robustness of type 1-specific gene expression and exemplifying how the miRNA-target gene relationship can be stably sustained in a variety of epithelial tumors.

Indexed as

Gene Expression Regulation, NeoplasticCarcinomaCarcinoma, Non-Small-Cell LungCaveolin 1Caveolin 2Cell Line, TumorEarly Growth Response Protein 1Gene Expression ProfilingGene Knockdown TechniquesHumansHyaluronan ReceptorsMicroRNAsModels, BiologicalProto-Oncogene Proteins c-metTranscription FactorsCAV1 protein, humanCAV2 protein, humanCaveolin 1Caveolin 2Early Growth Response Protein 1EGR1 protein, humanHyaluronan ReceptorsMicroRNAsmirn199 microRNA, humanProto-Oncogene Proteins c-metSMARCA2 protein, humanTranscription Factors

Identifiers

PMID25673149
PMCPMC4325331
OpenAlexW2169734926

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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.