Evidence map›Paper›PMID 19525223›Full record

ArticleThe Journal of biological chemistry2009

Scavenger chemokine (CXC motif) receptor 7 (CXCR7) is a direct target gene of HIC1 (hypermethylated in cancer 1).

Capucine Van Rechem, Brian R Rood, Majid Touka, Sébastien Pinte, Mathias Jenal, Cateline Guérardel, Keri Ramsey, Didier Monté, Agnès Bégue, Mario P Tschan and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

43 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
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  10. Oncotarget · 2020
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  14. Article
  15. Article
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  18. CXCR7 Targeting and Its Major Disease Relevance.Frontiers in pharmacology · 2018
    Review
  19. Article
  20. 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

12 authors at 7 institutions in 3 countries.

Capucine Van RechemCNRS UMR 8161 Institut de Biologie de Lille, Université de Lille NORD de France, Institut Pasteur de Lille, 59017 Lille, France.
Brian R Rood
Majid Touka
Sébastien Pinte
Mathias Jenal
Cateline Guérardel
Keri Ramsey
Didier Monté
Agnès Bégue
Mario P Tschan
Dietrich A Stephan
Dominique Leprince
Institut Pasteur de Lille · FRCentre National de la Recherche Scientifique · FRTranslational Genomics Research Institute · USUniversity of Bern · CHChildren's National · USInstitut de Biologie de Lille · FRUniversité de Lille · FR

Funding

Child Health Research Career Development Award (CHRCDA) Program at Children's NationalK12HD001399 · NICHD · CHILDREN'S RESEARCH INSTITUTE · PI NATHAN KUPPERMANN · 2001 to 2026
$9.1M
NICHD NIH HHS 5K12HD001399-05NICHD NIH HHS K12 HD001399
6 · The paper itself

Abstract

The tumor suppressor gene HIC1 (Hypermethylated in Cancer 1) that is epigenetically silenced in many human tumors and is essential for mammalian development encodes a sequence-specific transcriptional repressor. The few genes that have been reported to be directly regulated by HIC1 include ATOH1, FGFBP1, SIRT1, and E2F1. HIC1 is thus involved in the complex regulatory loops modulating p53-dependent and E2F1-dependent cell survival and stress responses. We performed genome-wide expression profiling analyses to identify new HIC1 target genes, using HIC1-deficient U2OS human osteosarcoma cells infected with adenoviruses expressing either HIC1 or GFP as a negative control. These studies identified several putative direct target genes, including CXCR7, a G-protein-coupled receptor recently identified as a scavenger receptor for the chemokine SDF-1/CXCL12. CXCR7 is highly expressed in human breast, lung, and prostate cancers. Using quantitative reverse transcription-PCR analyses, we demonstrated that CXCR7 was repressed in U2OS cells overexpressing HIC1. Inversely, inactivation of endogenous HIC1 by RNA interference in normal human WI38 fibroblasts results in up-regulation of CXCR7 and SIRT1. In silico analyses followed by deletion studies and luciferase reporter assays identified a functional and phylogenetically conserved HIC1-responsive element in the human CXCR7 promoter. Moreover, chromatin immunoprecipitation (ChIP) and ChIP upon ChIP experiments demonstrated that endogenous HIC1 proteins are bound together with the C-terminal binding protein corepressor to the CXCR7 and SIRT1 promoters in WI38 cells. Taken together, our results implicate the tumor suppressor HIC1 in the transcriptional regulation of the chemokine receptor CXCR7, a key player in the promotion of tumorigenesis in a wide variety of cell types.

Indexed as

AdenoviridaeAlcohol OxidoreductasesBase SequenceCell Line, TumorCell ProliferationChromatin ImmunoprecipitationConserved SequenceDNA-Binding ProteinsDown-RegulationFibroblastsGene Expression Regulation, NeoplasticGenes, NeoplasmGenetic VectorsHumansKruppel-Like Transcription FactorsMolecular Sequence DataACKR3 protein, humanAlcohol OxidoreductasesC-terminal binding proteinDNA-Binding ProteinsHIC1 protein, humanKruppel-Like Transcription FactorsReceptors, CXCRRNA, MessengerSIRT1 protein, humanSirtuin 1Sirtuins

Identifiers

PMID19525223
PMCPMC2742858
OpenAlexW1982882392

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.