Evidence map›Paper›PMID 21871017›Full record

ArticleThe Biochemical journal2011

NFAT promotes carcinoma invasive migration through glypican-6.

Gary K Yiu, Aura Kaunisto, Y Rebecca Chin, Alex Toker

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Proteogenomic Analysis of Coronary Artery Calcification in Human Populations.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. The Role of Glypicans in Cancer Progression and Therapy.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020
    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

4 authors at 2 institutions in 1 country.

Gary K YiuDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Aura Kaunisto
Y Rebecca Chin
Alex Toker
Beth Israel Deaconess Medical Center · USHarvard University · US

Funding

Training Program in Angiogenesis &InflammationT32HL007893 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI DVORAK, HAROLD FISHER · 1998 to 2017
$5.5M
Role of PLCgamma and NFAT Signaling Pathway in CarcinomaR01CA096710 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TOKER, ALEX · 2002 to 2013
$3.0M
NCI NIH HHS CA096710NCI NIH HHS R01 CA096710NHLBI NIH HHS T32HL007893
6 · The paper itself

Abstract

Invasive migration of carcinoma cells is a prerequisite for the metastatic dissemination of solid tumours. Numerous mechanisms control the ability of cancer cells to acquire a motile and invasive phenotype, and subsequently degrade and invade the basement membrane. Several genes that are up-regulated in breast carcinoma are responsible for mediating the metastatic cascade. Recent studies have revealed that the NFAT (nuclear factor of activated T-cells) is a transcription factor that is highly expressed in aggressive breast cancer cells and tissues, and mediates invasion through transcriptional induction of pro-invasion and migration genes. In the present paper we demonstrate that NFAT promotes breast carcinoma invasion through induction of GPC (glypican) 6, a cell-surface glycoprotein. NFAT transcriptionally regulates GPC6 induction in breast cancer cells and binds to three regulatory elements in the GPC6 proximal promoter. Expression of GPC6 in response to NFAT signalling promotes invasive migration, whereas GPC6 silencing with shRNA (small-hairpin RNA) potently blocks this phenotype. The mechanism by which GPC6 promotes invasive migration involves inhibition of canonical β-catenin and Wnt signalling, and up-regulation of non-canonical Wnt5A signalling leading to the activation of JNK (c-Jun N-terminal kinase) and p38 MAPK (mitogen-activated protein kinase). Thus GPC6 is a novel NFAT target gene in breast cancer cells that promotes invasive migration through Wnt5A signalling.

Indexed as

beta CateninBreast NeoplasmsCell Line, TumorCell MovementFemaleGlypicansHumansJNK Mitogen-Activated Protein KinasesNeoplasm InvasivenessNFATC Transcription Factorsp38 Mitogen-Activated Protein KinasesProto-Oncogene ProteinsTranscriptional ActivationWnt-5a ProteinWnt ProteinsWnt Signaling Pathwaybeta CateninGlypicansGPC6 protein, humanJNK Mitogen-Activated Protein KinasesNFATC1 protein, humanNFATC Transcription Factorsp38 Mitogen-Activated Protein KinasesProto-Oncogene ProteinsWnt-5a ProteinWNT5A protein, humanWnt Proteins

Identifiers

PMID21871017
PMCPMC3204871
OpenAlexW2092076185

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.