Evidence map›Paper›PMID 26065921›Full record

ArticleNature communications2015

Loss of microRNA-27b contributes to breast cancer stem cell generation by activating ENPP1.

Ryou-u Takahashi, Hiroaki Miyazaki, Fumitaka Takeshita, Yusuke Yamamoto, Kaho Minoura, Makiko Ono, Makoto Kodaira, Kenji Tamura, Masaki Mori, Takahiro Ochiya

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 2 pooled it
6.0field-weighted citation impact, top 3% 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

79 citing papers in PubMed, 2 syntheses or guidelines pooled it, 155 citations in OpenAlex.

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  15. ENPP1 is an innate immune checkpoint of the anticancer cGAMP-STING pathway in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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  18. ENPP1 Immunobiology as a Therapeutic Target.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Review
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19 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Ryou-u TakahashiDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute, 1-1, Tsukiji 5-chome, Tokyo 104-0045, Japan.
Hiroaki MiyazakiDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute, 1-1, Tsukiji 5-chome, Tokyo 104-0045, Japan.
Fumitaka TakeshitaDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute, 1-1, Tsukiji 5-chome, Tokyo 104-0045, Japan.
Yusuke YamamotoDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute, 1-1, Tsukiji 5-chome, Tokyo 104-0045, Japan.
Kaho MinouraGenomic Application Group, Japan Diagnostics and Genomics, Agilent Technologies Japan Ltd., 9-1, Tokyo 192-8510, Japan.
Makiko OnoDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute, 1-1, Tsukiji 5-chome, Tokyo 104-0045, Japan.
Makoto KodairaDepartment of Breast and Medical Oncology, National Cancer Center Hospital, 1-1, Tsukiji 5-chome, Tokyo 104-0045, Japan.
Kenji TamuraDepartment of Breast and Medical Oncology, National Cancer Center Hospital, 1-1, Tsukiji 5-chome, Tokyo 104-0045, Japan.
Masaki MoriDepartment of Gastroenterological Surgery, Graduated School of Medicine, Osaka University, Osaka 565-0871, Japan.
Takahiro OchiyaDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute, 1-1, Tsukiji 5-chome, Tokyo 104-0045, Japan.
Agilent Technologies (Japan) · JPOsaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer stem cells (CSCs) have been identified in various types of cancer; however, the mechanisms by which cells acquire CSC properties such as drug resistance and tumour seeding ability are not fully understood. Here, we identified microRNA-27b (miR-27b) as a key regulator for the generation of a side-population in breast cancer cells that showed CSC properties, and also found that the anti-type II diabetes (T2D) drug metformin reduced this side-population via miR-27b-mediated repression of ectonucleotide pyrophosphatase/phosphodiesterase family member 1 (ENPP1), which is involved in T2D development. ENPP1 induced the generation of the side-population via upregulation of the ABCG2 transporter. ENPP1 was also identified as a substrate of the 26S proteasome, the activity of which is downregulated in CSCs. Overall, these results demonstrate that a T2D-associated gene plays an important role in tumour development and that its expression is strictly controlled at the mRNA and protein levels.

Indexed as

Antineoplastic Agents, PhytogenicBreast NeoplasmsCell Line, TumorDocetaxelDown-RegulationFemaleHumansMicroRNAsNeoplastic Stem CellsPhosphoric Diester HydrolasesPyrophosphatasesTaxoidsAntineoplastic Agents, PhytogenicDocetaxelectonucleotide pyrophosphatase phosphodiesterase 1MicroRNAsMIRN27 microRNA, humanPhosphoric Diester HydrolasesPyrophosphatasesTaxoids

Identifiers

PMID26065921
PMCPMC4490376
OpenAlexW2231088500

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.