Evidence map›Paper›PMID 20924107›Full record

ArticleCancer research2010

Expression of the transcriptional repressor Gfi-1 is regulated by C/EBP{alpha} and is involved in its proliferation and colony formation-inhibitory effects in p210BCR/ABL-expressing cells.

Maria Rosa Lidonnici, Alessandra Audia, Angela Rachele Soliera, Marco Prisco, Giovanna Ferrari-Amorotti, Todd Waldron, Nick Donato, Ying Zhang, Robert V Martinez, Tessa L Holyoake and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2010. 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
1.3field-weighted citation impact, top 17% 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, 30 citations in OpenAlex.

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  13. Selecting the best frontline treatment in chronic myeloid leukemia.Current hematologic malignancy reports · 2015
    Review
  14. Article
  15. C/EBPα in normal and malignant myelopoiesis.International journal of hematology · 2015
    Review
  16. Article
  17. Article
  18. Article
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  20. Article
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

11 authors at 5 institutions in 3 countries.

Maria Rosa LidonniciDepartment of Cancer Biology and Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Alessandra Audia
Angela Rachele Soliera
Marco Prisco
Giovanna Ferrari-Amorotti
Todd Waldron
Nick Donato
Ying Zhang
Robert V Martinez
Tessa L Holyoake
Bruno Calabretta
University of Glasgow · GBGartnavel General Hospital · GBMichigan Center for Translational Pathology · USThomas Jefferson University · USUniversity of Michigan–Ann Arbor · US

Funding

TRAIL Receptors in Apoptosis and CancerP01CA078890 · NCI · THOMAS JEFFERSON UNIVERSITY · PI CALABRETTA, BRUNO · 1999 to 2007
$8.9M
TRANSCRIPTION FACTOR REGULATION BY THE BCR/ABL ONCOGENER01CA095111 · NCI · THOMAS JEFFERSON UNIVERSITY · PI CALABRETTA, BRUNO · 2002 to 2012
$2.8M
NCI NIH HHS CA 95111NCI NIH HHS P01 CA078890NCI NIH HHS R01 CA095111PHS HHS P01 78890
6 · The paper itself

Abstract

Ectopic expression of CAAT/enhancer binding protein α (C/EBPα) in p210BCR/ABL-expressing cells induces granulocytic differentiation, inhibits proliferation, and suppresses leukemogenesis. To dissect the molecular mechanisms underlying these biological effects, C/EBPα-regulated genes were identified by microarray analysis in 32D-p210BCR/ABL cells. One of the genes whose expression was activated by C/EBPα in a DNA binding-dependent manner in BCR/ABL-expressing cells is the transcriptional repressor Gfi-1. We show here that C/EBPα interacts with a functional C/EBP binding site in the Gfi-1 5'-flanking region and enhances the promoter activity of Gfi-1. Moreover, in K562 cells, RNA interference-mediated downregulation of Gfi-1 expression partially rescued the proliferation-inhibitory but not the differentiation-inducing effect of C/EBPα. Ectopic expression of wild-type Gfi-1, but not of a transcriptional repressor mutant (Gfi-1P2A), inhibited proliferation and markedly suppressed colony formation but did not induce granulocytic differentiation of BCR/ABL-expressing cells. By contrast, Gfi-1 short hairpin RNA-tranduced CD34(+) chronic myeloid leukemia cells were markedly more clonogenic than the scramble-transduced counterpart. Together, these studies indicate that Gfi-1 is a direct target of C/EBPα required for its proliferation and survival-inhibitory effects in BCR/ABL-expressing cells.

Indexed as

CCAAT-Enhancer-Binding Protein-alphaCCAAT-Enhancer-Binding ProteinsCell DifferentiationCell DivisionColony-Forming Units AssayDNA-Binding ProteinsDNA PrimersDown-RegulationFusion Proteins, bcr-ablGene AmplificationGene Expression RegulationGenes, ReporterHumansInverted Repeat SequencesK562 CellsLuciferasesCCAAT-Enhancer-Binding Protein-alphaCCAAT-Enhancer-Binding ProteinsCEBPA protein, humanDNA-Binding ProteinsDNA PrimersFusion Proteins, bcr-ablGFI1 protein, humanLuciferasesTranscription Factors

Identifiers

PMID20924107
PMCPMC2955805
OpenAlexW2154238201

What OpenQuestion holds

Textmetadata
LicenceTDM
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.