Evidence map›Paper›PMID 20473547›Full record

ArticleCellular and molecular life sciences : CMLS2010

HDAC3 selectively represses CREB3-mediated transcription and migration of metastatic breast cancer cells.

Han-Cheon Kim, Kyung-Chul Choi, Hyo-Kyoung Choi, Hee-Bum Kang, Mi-Jeong Kim, Yoo-Hyun Lee, Ok-Hee Lee, Jeongmin Lee, Young Jun Kim, Woojin Jun and 2 more

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

40 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
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  7. Review
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  9. CXCL12 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Targeting CXCL12/CXCR4 Axis in Tumor Immunotherapy.Current medicinal chemistry · 2019
    Review
  15. Review
  16. Role of HDAC3-miRNA-CAGE Network in Anti-Cancer Drug-Resistance.International journal of molecular sciences · 2018
    Review
  17. Article
  18. Article
  19. Article
  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

12 authors at 7 institutions in 2 countries.

Han-Cheon KimDepartment of Biochemistry and Molecular Biology, Center for Chronic Metabolic Disease Research, Brain Korea 21 Project for Medical Sciences, Severance Medical Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Kyung-Chul Choi
Hyo-Kyoung Choi
Hee-Bum Kang
Mi-Jeong Kim
Yoo-Hyun Lee
Ok-Hee Lee
Jeongmin Lee
Young Jun Kim
Woojin Jun
Jae-Wook Jeong
Ho-Geun Yoon
Yonsei University · KRBaylor College of Medicine · USChonnam National University · KRKorea University · KRKyung Hee University Medical Center · KRSeverance Hospital · KRUniversity of Suwon · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We identified CREB3 as a novel HDAC3-interacting protein in a yeast two-hybrid screen for HDAC3-interacting proteins. Among all class I HDACs, CREB3 specifically interacts with HDAC3, in vitro and in vivo. HDAC3 efficiently inhibited CREB3-enhanced NF-κB activation, whereas the other class I HDACs did not alter NF-κB-dependent promoter activities or the expression of NF-κB target genes. Importantly, both knock-down of CREB3 and overexpression of HDAC3 suppressed the transcriptional activation of the novel CREB3-regulated gene, CXCR4. Furthermore, CREB3 was shown to bind to the CRE element in the CXCR4 promoter and to activate the transcription of the CXCR4 gene by causing dissociation of HDAC3 and subsequently increasing histone acetylation. Importantly, both the depletion of HDAC3 and the overexpression of CREB3 substantially increased the migration of MDA-MB-231 metastatic breast cancer cells. Taken together, these findings suggest that HDAC3 selectively represses CREB3-mediated transcriptional activation and chemotactic signalling in human metastatic breast cancer cells.

Indexed as

Cell MovementTranscription, GeneticBreast NeoplasmsCell Line, TumorCyclic AMP Response Element-Binding ProteinDown-RegulationFemaleGene Expression Regulation, NeoplasticHistone Deacetylase 3Histone DeacetylasesHumansNeoplasm MetastasisNF-kappa BProtein BindingProtein Interaction MappingProtein Structure, TertiaryCREB3 protein, humanCXCR4 protein, humanCyclic AMP Response Element-Binding ProteinHistone Deacetylase 3Histone DeacetylasesNF-kappa BReceptors, CXCR4Repressor Proteins

Identifiers

PMID20473547
PMCPMC11115716
OpenAlexW2002554985

What OpenQuestion holds

Textmetadata
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.