Evidence map›Paper›PMID 22132193›Full record

ArticlePloS one2011

Transcriptional repression of Cdc25B by IER5 inhibits the proliferation of leukemic progenitor cells through NF-YB and p300 in acute myeloid leukemia.

Satoki Nakamura, Yasuyuki Nagata, Lin Tan, Tomonari Takemura, Kiyoshi Shibata, Michio Fujie, Shinya Fujisawa, Yasutaka Tanaka, Mitsuo Toda, Reiko Makita and 6 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

21 citing papers in PubMed, 44 citations in OpenAlex.

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  9. HighFrontiers in cell and developmental biology · 2021
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  12. ChickenOncotarget · 2017
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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

16 authors at 4 institutions in 1 country.

Satoki NakamuraDepartment of Internal Medicine III, Hamamatsu University School of Medicine, Higashi-ku, Hamamatsu, Shizuoka, Japan. satonaka@hama-med.ac.jp
Yasuyuki Nagata
Lin Tan
Tomonari Takemura
Kiyoshi Shibata
Michio Fujie
Shinya Fujisawa
Yasutaka Tanaka
Mitsuo Toda
Reiko Makita
Kenji Tsunekawa
Manabu Yamada
Mayumi Yamaoka
Junko Yamashita
Kazunori Ohnishi
Mitsuji Yamashita
Shizuoka University · JPHamamatsu University School of Medicine · JPHamamatsu Medical Center · JPHamamatsu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immediately-early response gene 5 (IER5) has been reported to be induced by γ-ray irradiation and to play a role in the induction of cell death caused by radiation. We previously identified IER5 as one of the 2,3,4-tribromo-3-methyl-1-phenylphospholane 1-oxide (TMPP)-induced transcriptional responses in AML cells, using microarrays that encompassed the entire human genome. However, the biochemical pathway and mechanisms of IER5 function in regulation of the cell cycle remain unclear. In this study, we investigated the involvement of IER5 in the cell cycle and in cell proliferation of acute myeloid leukemia (AML) cells. We found that the over-expression of IER5 in AML cell lines and in AML-derived ALDH(hi) (High Aldehyde Dehydrogenase activity)/CD34(+) cells inhibited their proliferation compared to control cells, through induction of G2/M cell cycle arrest and a decrease in Cdc25B expression. Moreover, the over-expression of IER5 reduced colony formation of AML-derived ALDH(hi)/CD34(+) cells due to a decrease in Cdc25B expression. In addition, over-expression of Cdc25B restored TMPP inhibitory effects on colony formation in IER5-suppressed AML-derived ALDH(hi)/CD34(+) cells. Furthermore, the IER5 reduced Cdc25B mRNA expression through direct binding to Cdc25B promoter and mediated its transcriptional attenuation through NF-YB and p300 transcriptinal factors. In summary, we found that transcriptional repression mediated by IER5 regulates Cdc25B expression levels via the release of NF-YB and p300 in AML-derived ALDH(hi)/CD34(+) cells, resulting in inhibition of AML progenitor cell proliferation through modulation of cell cycle. Thus, the induction of IER5 expression represents an attractive target for AML therapy.

Indexed as

Transcription, GeneticAntigens, CD34CCAAT-Binding Factorcdc25 PhosphatasesCell CycleCell ProliferationCell SeparationE1A-Associated p300 ProteinGene Expression Regulation, LeukemicGene Knockdown TechniquesHumansImmediate-Early ProteinsLeukemia, Myeloid, AcuteNeoplastic Stem CellsNuclear ProteinsPromoter Regions, GeneticAntigens, CD34CCAAT-Binding Factorcdc25 PhosphatasesE1A-Associated p300 ProteinEP300 protein, humanIER5 protein, humanImmediate-Early ProteinsNFYB protein, humanNuclear ProteinsRepressor ProteinsRNA, Messenger

Identifiers

PMID22132193
PMCPMC3223216
OpenAlexW1995108968

What Socratic 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 Socratic graph.