Evidence map›Paper›PMID 18628953›Full record

ArticlePloS one2008

Role of Sox-9, ER81 and VE-cadherin in retinoic acid-mediated trans-differentiation of breast cancer cells.

Yoshimi Endo, Kamla Deonauth, Priya Prahalad, Becky Hoxter, Yuelin Zhu, Stephen W Byers

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. SOX9: an important factor in regulating breast cancer.European journal of medical research · 2025
    Review
  2. Review
  3. Review
  4. Review
  5. PGE2 signaling and its biosynthesis-related enzymes in cholangiocarcinoma progression.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Cancer stem cells and hepatocellular carcinoma.Cancer biology & therapy · 2009
    Review
  15. Liver stem cells and hepatocellular carcinoma.Hepatology (Baltimore, Md.) · 2009
    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

6 authors at 3 institutions in 1 country.

Yoshimi EndoLombardi Comprehensive Cancer Center, Department of Oncology, Georgetown University, Washington DC, United States of America.
Kamla Deonauth
Priya Prahalad
Becky Hoxter
Yuelin Zhu
Stephen W Byers
Georgetown University Medical Center · USGeorgetown University · USHoward University · US

Funding

Folate, 1-Carbon Nutrients, Gene Variants &Colon CancerU54CA100971 · NCI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI HUNTER, DAVID JOHN · 2003 to 2008
$7.0M
Beta-catenin-specific regulation of the vitamin D pathway in colon cancerR01CA129813 · NCI · GEORGETOWN UNIVERSITY · PI BYERS, STEPHEN W · 2008 to 2012
$1.6M
Cross Regulation of Beta-catenin and Retinoid SignalingR01DK058196 · NIDDK · GEORGETOWN UNIVERSITY · PI BYERS, STEPHEN W · 2002 to 2004
$844k
NCI NIH HHS CA129813NCI NIH HHS R01 CA129813NCI NIH HHS U54 CA100971NCI NIH HHS U54CA100971NIDDK NIH HHS DK058196
6 · The paper itself

Abstract

Many aspects of development, tumor growth and metastasis depend upon the provision of an adequate vasculature. This can be a result of regulated angiogenesis, recruitment of circulating endothelial progenitors and/or vascular trans-differentiation. The present study demonstrates that treatment of SKBR-3 breast cancer cells with retinoic acid (RA), an important regulator of embryogenesis, cancer and other diseases, stimulates the formation of networks in Matrigel. RA-treatment of SKBR-3 cells co-cultured with human umbilical vein endothelial cells resulted in the formation of mixed structures. RA induces expression of many endothelial genes including vascular endothelial (VE) cadherin. VE-cadherin was also induced by RA in a number of other breast cancer cells. We show that RA-induced VE-cadherin is responsible for the RA-induced morphological changes. RA rapidly induced the expression of Sox-9 and ER81, which in turn form a complex on the VE-cadherin promoter and are required to mediate the transcriptional regulation of VE-cadherin by RA. These data indicate that RA may promote the expression of endothelial genes resulting in endothelial-like differentiation, or provide a mechanism whereby circulating endothelial progenitor cells could be incorporated into a growing organ or tumor.

Indexed as

Gene Expression Regulation, NeoplasticAntigens, CDBreast NeoplasmsCadherin 5CadherinsCell DifferentiationCell Line, TumorCell TransdifferentiationCollagenDNA-Binding ProteinsDrug CombinationsHigh Mobility Group ProteinsHumansLamininModels, BiologicalNeovascularization, PathologicAntigens, CDCadherin 5CadherinsCollagenDNA-Binding ProteinsDrug CombinationsETV1 protein, humanHigh Mobility Group ProteinsLamininmatrigelProteoglycansSOX9 protein, humanSOX9 Transcription FactorTranscription FactorsTretinoin

Identifiers

PMID18628953
PMCPMC2444023
OpenAlexW1972766112

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.