Evidence map›Paper›PMID 18801183›Full record

ArticleBMC cancer2008

Expression profile of CREB knockdown in myeloid leukemia cells.

Matteo Pellegrini, Jerry C Cheng, Jon Voutila, Dejah Judelson, Julie Taylor, Stanley F Nelson, Kathleen M Sakamoto

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2008. 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
0.6field-weighted citation impact, top 33% 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, 33 citations in OpenAlex.

  1. cAMP response element-binding protein promotes gliomagenesis by modulating the expression of oncogenic microRNA-23a.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Trial
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  9. Inhibition of Ras-mediated signaling pathways in CML stem cells.Cellular oncology (Dordrecht, Netherlands) · 2015
    Review
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  11. Article
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  16. Article
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  19. CREB and leukemogenesis.Critical reviews in oncogenesis · 2011
    Review
  20. CREB in the pathophysiology of cancer: implications for targeting transcription factors for cancer therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009
    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

7 authors at 3 institutions in 1 country.

Matteo PellegriniDepartment of Molecular, Cellular, and Developmental Biology, University of California, Los Angeles, USA. matteop@mcdb.ucla.edu
Jerry C Cheng
Jon Voutila
Dejah Judelson
Julie Taylor
Stanley F Nelson
Kathleen M Sakamoto
Kaiser Permanente West Los Angeles Medical Center · USUniversity of California, Los Angeles · USCalifornia Institute of Technology · US

Funding

The Role of CREB in Normal Myelopoiesis and LeukemogenesisR01HL075826 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SAKAMOTO, KATHLEEN M · 2004 to 2013
$3.2M
UCLA NHLBI Shared Microarray FacilitiesR01HL072367 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI NELSON, STANLEY F. · 2002 to 2005
$3.0M
Molecular and Cellular Characterization of Myeloproliferative DiseaseR01HL083077 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SAKAMOTO, KATHLEEN M · 2005 to 2010
$1.5M
Role of CREB in Normal Hematopoiesis and AMLF32HL085013 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHENG, JERRY C · 2006 to 2006
$54k
NHLBI NIH HHS F32 HL085013NHLBI NIH HHS F32HL085013NHLBI NIH HHS HL75826NHLBI NIH HHS HL83077NHLBI NIH HHS R01 HL072367NHLBI NIH HHS R01 HL075826NHLBI NIH HHS R01 HL083077NHLBI NIH HHS R01HL72367
6 · The paper itself

Abstract

backgroundThe cAMP Response Element Binding Protein, CREB, is a transcription factor that regulates cell proliferation, differentiation, and survival in several model systems, including neuronal and hematopoietic cells. We demonstrated that CREB is overexpressed in acute myeloid and leukemia cells compared to normal hematopoietic stem cells. CREB knockdown inhibits leukemic cell proliferation in vitro and in vivo, but does not affect long-term hematopoietic reconstitution.

methodsTo understand downstream pathways regulating CREB, we performed expression profiling with RNA from the K562 myeloid leukemia cell line transduced with CREB shRNA.

resultsBy combining our expression data from CREB knockdown cells with prior ChIP data on CREB binding we were able to identify a list of putative CREB regulated genes. We performed extensive analyses on the top genes in this list as high confidence CREB targets. We found that this list is enriched for genes involved in cancer, and unexpectedly, highly enriched for histone genes. Furthermore, histone genes regulated by CREB were more likely to be specifically expressed in hematopoietic lineages. Decreased expression of specific histone genes was validated in K562, TF-1, and primary AML cells transduced with CREB shRNA.

conclusionWe have identified a high confidence list of CREB targets in K562 cells. These genes allow us to begin to understand the mechanisms by which CREB contributes to acute leukemia. We speculate that regulation of histone genes may play an important role by possibly altering the regulation of DNA replication during the cell cycle.

Indexed as

Gene Expression ProfilingGene Expression Regulation, LeukemicGene Knockdown TechniquesCell LineCell ProliferationCyclic AMP Response Element-Binding ProteinGene Regulatory NetworksGenes, cdcGenes, NeoplasmHistonesHumansK562 CellsLeukemia, MyeloidResponse ElementsCyclic AMP Response Element-Binding ProteinHistones

Identifiers

PMID18801183
PMCPMC2647550
OpenAlexW2101004371

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.