Evidence map›Paper›PMID 23038246›Full record

ArticleThe Journal of biological chemistry2012

β-Catenin activates the HOXA10 and CDX4 genes in myeloid progenitor cells.

Ling Bei, Chirag Shah, Hao Wang, Weiqi Huang, Rupali Roy, Elizabeth A Eklund

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

13 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Regulation of HOX gene expression in AML.Blood cancer journal · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. HOXA10 controls proliferation, migration and invasion in oral squamous cell carcinoma.International journal of clinical and experimental pathology · 2015
    Article
  13. 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

6 authors at 2 institutions in 1 country.

Ling BeiFeinberg School of Medicine and the Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois 60611, USA.
Chirag Shah
Hao Wang
Weiqi Huang
Rupali Roy
Elizabeth A Eklund
Northwestern University · USJesse Brown VA Medical Center · US

Funding

HoxA10 Function During Myeloid DifferentiationR01HL087717 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI EKLUND, ELIZABETH ANN · 2007 to 2011
$1.9M
Triad1 regulates myelopoiesis and functions as a leukemia suppressorR01CA195642 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI EKLUND, ELIZABETH ANN · 2015 to 2019
$1.8M
NCI NIH HHS R01 CA195642NHLBI NIH HHS R01 HL087717NHLBI NIH HHS R01-HL87717
6 · The paper itself

Abstract

HoxA10 is a homeodomain transcription factor that is involved in maintenance of the myeloid progenitor population and implicated in myeloid leukemogenesis. Previously, we found that FGF2 and CDX4 are direct target genes of HoxA10 and that HOXA10 is a Cdx4 target gene. We also found that increased production of fibroblast growth factor 2 (Fgf2) by HoxA10-overexpressing myeloid progenitor cells results in activation of β-catenin in an autocrine manner. In this study, we identify novel cis elements in the CDX4 and HOXA10 genes that are activated by β-catenin in myeloid progenitor cells. We determine that β-catenin interacts with these cis elements, identifying both CDX4 and HOXA10 as β-catenin target genes in this context. We demonstrate that HoxA10-induced CDX4 transcription is influenced by Fgf2-dependent β-catenin activation. Similarly, Cdx4-induced HOXA10 transcription is influenced by β-catenin in an Fgf2-dependent manner. Increased expression of a set of Hox proteins, including HoxA10, is associated with poor prognosis in acute myeloid leukemia. Cdx4 contributes to leukemogenesis in Hox-overexpressing acute myeloid leukemia, and increased β-catenin activity is also associated with poor prognosis. The current studies identify a molecular mechanisms through which increased expression of HoxA10 increases Cdx4 expression by direct CDX4 activation and by Fgf2-induced β-catenin activity. This results in Cdx4-induced HoxA10-expression, creating a positive feedback mechanism.

Indexed as

Animalsbeta CateninFibroblast Growth Factor 2Gene Expression RegulationHomeobox A10 ProteinsHomeodomain ProteinsHumansMiceMice, KnockoutMyeloid Progenitor CellsResponse ElementsTranscription, GeneticU937 Cellsbeta CateninCdx4 protein, mouseFibroblast Growth Factor 2Homeobox A10 ProteinsHomeodomain ProteinsHOXA10 protein, humanHoxa10 protein, mouse

Identifiers

PMID23038246
PMCPMC3501069
OpenAlexW2006960606

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.