Evidence map›Paper›PMID 25072246›Full record

ArticlePloS one2014

A PU.1 suppressive target gene, metallothionein 1G, inhibits retinoic acid-induced NB4 cell differentiation.

Naomi Hirako, Hiroko Nakano, Shinichiro Takahashi

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 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.1field-weighted citation impact, top 44% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. The roles of metallothioneins in carcinogenesis.Journal of hematology & oncology · 2018
    Review
  8. Review
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

3 authors at 1 institution in 1 country.

Naomi HirakoDivision of Molecular Hematology, Kitasato University Graduate School of Medical Sciences, Minami-ku, Sagamihara, Japan.
Hiroko NakanoDivision of Hematology, Kitasato University School of Allied Health Sciences, Minami-ku, Sagamihara, Japan.
Shinichiro TakahashiDivision of Molecular Hematology, Kitasato University Graduate School of Medical Sciences, Minami-ku, Sagamihara, Japan; Division of Hematology, Kitasato University School of Allied Health Sciences, Minami-ku, Sagamihara, Japan.
Kitasato University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We recently revealed that myeloid master regulator SPI1/PU.1 directly represses metallothionein (MT) 1G through its epigenetic activity of PU.1, but the functions of MT1G in myeloid differentiation remain unknown. To clarify this, we established MT1G-overexpressing acute promyelocytic leukemia NB4 (NB4MTOE) cells, and investigated whether MT1G functionally contributes to all-trans retinoic acid (ATRA)-induced NB4 cell differentiation. Real-time PCR analyses demonstrated that the inductions of CD11b and CD11c and reductions in myeloperoxidase and c-myc by ATRA were significantly attenuated in NB4MTOE cells. Morphological examination revealed that the percentages of differentiated cells induced by ATRA were reduced in NB4MTOE cells. Since G1 arrest is a hallmark of ATRA-induced NB4 cell differentiation, we observed a decrease in G1 accumulation, as well as decreases in p21WAF1/CIP1 and cyclin D1 inductions, by ATRA in NB4MTOE cells. Nitroblue tetrazolium (NBT) reduction assays revealed that the proportions of NBT-positive cells were decreased in NB4MTOE cells in the presence of ATRA. Microarray analyses showed that the changes in expression of several myeloid differentiation-related genes (GATA2, azurocidin 1, pyrroline-5-carboxylate reductase 1, matrix metallopeptidase -8, S100 calcium-binding protein A12, neutrophil cytosolic factor 2 and oncostatin M) induced by ATRA were disturbed in NB4MTOE cells. Collectively, overexpression of MT1G inhibits the proper differentiation of myeloid cells.

Indexed as

Gene Expression RegulationAntigens, CDCell DifferentiationCell Line, TumorG1 Phase Cell Cycle CheckpointsGene ExpressionGene Expression ProfilingHumansImmunophenotypingLeukemia, Promyelocytic, AcuteMetallothioneinProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Reproducibility of ResultsTrans-ActivatorsTretinoinAntigens, CDMetallothioneinMT1G protein, humanProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-ActivatorsTretinoin

Identifiers

PMID25072246
PMCPMC4114787
OpenAlexW2170010347

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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.