Evidence map›Paper›PMID 23919497›Full record

ArticleThe Biochemical journal2013

A mechanism for epithelial-mesenchymal transition and anoikis resistance in breast cancer triggered by zinc channel ZIP6 and STAT3 (signal transducer and activator of transcription 3).

Christer Hogstrand, Peter Kille, Margaret Leigh Ackland, Stephen Hiscox, Kathryn M Taylor

Open access · hybridAbstract read
In one paragraph

Article in The Biochemical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
9.5field-weighted citation impact, top 1% 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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 142 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. ZIP-ZnT1 complexes mediate a local ZnCellular and molecular life sciences : CMLS · 2026
    Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Metal Ion Signaling in Biomedicine.Chemical reviews · 2025
    Review
  17. JAK-STAT Signaling in Autoimmunity and Cancer.ImmunoTargets and therapy · 2025
    Review
  18. Review
  19. Review
  20. Review

13 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Christer Hogstrand*Nutritional Sciences Division, King's College London, 3.85 Franklin-Wilkins Building, 150 Stamford Street, London SE1 9NH, U.K.
Peter Kille
Margaret Leigh Ackland
Stephen Hiscox
Kathryn M Taylor
Deakin University · AU

Funding

Wellcome Trust 091991/Z/10/Z
6 · The paper itself

Abstract

Genes involved in normal developmental processes attract attention as mediators of tumour progression as they facilitate migration of tumour cells. EMT (epithelial-mesenchymal transition), an essential part of embryonic development, tissue remodelling and wound repair, is crucial for tumour metastasis. Previously, zinc transporter ZIP6 [SLC39A6; solute carrier family 39 (zinc transporter), member 6; also known as LIV-1) was linked to EMT in zebrafish gastrulation through a STAT3 (signal transducer and activator of transcription 3) mechanism, resulting in nuclear localization of transcription factor Snail. In the present study, we show that zinc transporter ZIP6 is transcriptionally induced by STAT3 and unprecedented among zinc transporters, and is activated by N-terminal cleavage which triggers ZIP6 plasma membrane location and zinc influx. This zinc influx inactivates GSK-3β (glycogen synthase kinase 3β), either indirectly or directly via Akt or GSK-3β respectively, resulting in activation of Snail, which remains in the nucleus and acts as a transcriptional repressor of E-cadherin (epithelial cadherin), CDH1, causing cell rounding and detachment. This was mirrored by ZIP6-transfected cells which underwent EMT, detached from monolayers and exhibited resistance to anoikis by their ability to continue proliferating even after detachment. Our results indicate a causative role for ZIP6 in cell motility and migration, providing ZIP6 as a new target for prediction of clinical cancer spread and also suggesting a ZIP6-dependent mechanism of tumour metastasis.

Indexed as

AnimalsBreast NeoplasmsCadherinsCation Transport ProteinsCell Line, TumorCHO CellsCricetulusEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansNeoplasm ProteinsSignal TransductionSTAT3 Transcription FactorCadherinsCation Transport ProteinsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanNeoplasm ProteinsSLC39A6 protein, humanSTAT3 Transcription Factor

Identifiers

PMID23919497
PMCPMC3789231
OpenAlexW2095208806

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.