Evidence map›Paper›PMID 20981476›Full record

ArticleClinical & experimental metastasis2011

Endoglin suppresses human prostate cancer metastasis.

Minalini Lakshman, Xiaoke Huang, Vijayalakshmi Ananthanarayanan, Borko Jovanovic, Yueqin Liu, Clarissa S Craft, Diana Romero, Calvin P H Vary, Raymond C Bergan

Open access · greenAbstract read
In one paragraph

Article in Clinical & experimental metastasis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 46 citations in OpenAlex.

  1. JUNB and JUND in Urological Cancers: A Literature Review.Current issues in molecular biology · 2025
    Review
  2. Article
  3. Article
  4. Article
  5. Endoglin in the Spotlight to Treat Cancer.International journal of molecular sciences · 2021
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Cancer incidence in patients with hereditary hemorrhagic telangiectasia.Journal of cancer research and clinical oncology · 2017
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  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

9 authors at 5 institutions in 3 countries.

Minalini LakshmanDepartment of Medicine, Northwestern University Medical School, Lurie 6-105, 303 E. Superior Street, Chicago, IL 60611, USA.
Xiaoke Huang
Vijayalakshmi Ananthanarayanan
Borko Jovanovic
Yueqin Liu
Clarissa S Craft
Diana Romero
Calvin P H Vary
Raymond C Bergan
Northwestern University · USMaine Medical Center · USOntario Institute for Cancer Research · CARobert H. Lurie Comprehensive Cancer Center of Northwestern UniversityUniversity of Chicago · US

Funding

SUPPRESSIVE ROLE OF ANDROGEN RESPONSE GENE CALRETICULIN IN PROSTATE CANCERP50CA090386 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CRAWFORD, SUSAN · 2001 to 2013
$25.1M
Genistein-mediated Regulation of Prostate Cancer Cell MotilityR01CA122985 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BERGAN, RAYMOND C. · 2008 to 2012
$1.6M
NCI NIH HHS CA122985NCI NIH HHS CA90386NCI NIH HHS P50 CA090386NCI NIH HHS R01 CA122985
6 · The paper itself

Abstract

Endoglin is a transmembrane receptor that suppresses human prostate cancer (PCa) cell invasion. Small molecule therapeutics now being tested in humans can activate endoglin signaling. It is not known whether endoglin can regulate metastatic behavior, PCa tumor growth, nor what signaling pathways are linked to these processes. This study sought to investigate the effect of endoglin on these parameters. We used a murine orthotopic model of human PCa metastasis, designed by us to measure effects at early steps in the metastatic cascade, and implanted PCa cells stably engineered to express differing levels of endoglin. We now extend this model to measure cancer cells circulating in the blood. Progressive endoglin loss led to progressive increases in the number of circulating PCa cells as well as to the formation of soft tissue metastases. Endoglin was known to suppress invasion by activating the Smad1 transcription factor. We now show that it selectively activates specific Smad1-responsive genes, including JUNB, STAT1, and SOX4. Increased tumor growth and increased Ki67 expression in tissue was seen only with complete endoglin loss. By showing that endoglin increased TGFβ-mediated suppression of cell growth in vitro and TGFβ-mediated signaling in tumor tissue, loss of this growth-suppressive pathway appears to be implicated at least in part for the increased size of endoglin-deficient tumors. Endoglin is shown for the first time to suppress cell movement out of primary tumor as well as the formation of distant metastasis. It is also shown to co-regulate tumor growth and metastatic behavior in human PCa.

Indexed as

AnimalsAntigens, CDCell ProliferationDisease Models, AnimalEndoglinHumansImmunohistochemistryMaleMiceMice, Inbred BALB CNeoplasm InvasivenessNeoplasm MetastasisProstatic NeoplasmsReceptors, Cell SurfaceSignal TransductionSmad1 ProteinAntigens, CDEndoglinENG protein, humanReceptors, Cell SurfaceSmad1 ProteinTransforming Growth Factor beta

Identifiers

PMID20981476
PMCPMC3046557
OpenAlexW2034511793

What OpenQuestion holds

Textmetadata
LicenceTDM
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.