Evidence map›Paper›PMID 24037528›Full record

ArticleOncogene2014

MiR-200 can repress breast cancer metastasis through ZEB1-independent but moesin-dependent pathways.

X Li, S Roslan, C N Johnstone, J A Wright, C P Bracken, M Anderson, A G Bert, L A Selth, R L Anderson, G J Goodall and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 5 pooled it
5.4field-weighted citation impact, top 4% 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

86 citing papers in PubMed, 5 syntheses or guidelines pooled it, 124 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
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  14. Corneal injury repair and the potential involvement of ZEB1.Eye and vision (London, England) · 2024
    Review
  15. MicroRNA Expression Profile in Early-Stage Breast Cancers.MicroRNA (Shariqah, United Arab Emirates) · 2024
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  16. Article
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  20. Article

26 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

12 authors at 4 institutions in 1 country.

X LiDivision of Human Immunology, Centre for Cancer Biology, SA Pathology, Adelaide, South Australia, Australia.
S RoslanDivision of Human Immunology, Centre for Cancer Biology, SA Pathology, Adelaide, South Australia, Australia.
C N Johnstone1] Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne, Victoria, Australia [2] Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, Victoria, Australia [3] Department of Pathology, The University of Melbourne, Parkville, Victoria, Australia [4] Department of Pharmacology, The University of Melbourne, Parkville, Victoria, Australia.
J A Wright1] Division of Human Immunology, Centre for Cancer Biology, SA Pathology, Adelaide, South Australia, Australia [2] Discipline of Medicine, The University of Adelaide, Adelaide, South Australia, Australia.
C P Bracken1] Division of Human Immunology, Centre for Cancer Biology, SA Pathology, Adelaide, South Australia, Australia [2] Discipline of Medicine, The University of Adelaide, Adelaide, South Australia, Australia.
M AndersonDivision of Human Immunology, Centre for Cancer Biology, SA Pathology, Adelaide, South Australia, Australia.
A G BertDivision of Human Immunology, Centre for Cancer Biology, SA Pathology, Adelaide, South Australia, Australia.
L A SelthDame Roma Mitchell Cancer Research Laboratories, Discipline of Medicine, University of Adelaide, Hanson Institute, Adelaide, South Australia, Australia.
R L Anderson1] Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne, Victoria, Australia [2] Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, Victoria, Australia [3] Department of Pathology, The University of Melbourne, Parkville, Victoria, Australia.
G J Goodall1] Division of Human Immunology, Centre for Cancer Biology, SA Pathology, Adelaide, South Australia, Australia [2] Discipline of Medicine, The University of Adelaide, Adelaide, South Australia, Australia [3] School of Molecular and Biomedical Science, The University of Adelaide, Adelaide, South Australia, Australia.
P A Gregory1] Division of Human Immunology, Centre for Cancer Biology, SA Pathology, Adelaide, South Australia, Australia [2] Discipline of Medicine, The University of Adelaide, Adelaide, South Australia, Australia.
Y Khew-Goodall1] Division of Human Immunology, Centre for Cancer Biology, SA Pathology, Adelaide, South Australia, Australia [2] School of Molecular and Biomedical Science, The University of Adelaide, Adelaide, South Australia, Australia.
Centre for Cancer Biology · AUSouth Australia Pathology · AUPeter MacCallum Cancer Centre · AUHanson Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The microRNA-200 (miR-200) family has a critical role in regulating epithelial-mesenchymal transition and cancer cell invasion through inhibition of the E-cadherin transcriptional repressors ZEB1 and ZEB2. Recent studies have indicated that the miR-200 family may exert their effects at distinct stages in the metastatic process, with an overall effect of enhancing metastasis in a syngeneic mouse breast cancer model. We find in a xenograft orthotopic model of breast cancer metastasis that ectopic expression of members of the miR-200b/200c/429, but not the miR-141/200a, functional groups limits tumour cell invasion and metastasis. Despite modulation of the ZEB1-E-cadherin axis, restoration of ZEB1 in miR-200b-expressing cells was not able to alter metastatic potential suggesting that other targets contribute to this process. Instead, we found that miR-200b repressed several actin-associated genes, with the knockdown of the ezrin-radixin-moesin family member moesin alone phenocopying the repression of cell invasion by miR-200b. Moesin was verified to be directly targeted by miR-200b, and restoration of moesin in miR-200b-expressing cells was sufficient to alleviate metastatic repression. In breast cancer cell lines and patient samples, the expression of moesin significantly inversely correlated with miR-200 expression, and high levels of moesin were associated with poor relapse-free survival. These findings highlight the context-dependent effects of miR-200 in breast cancer metastasis and demonstrate the existence of a moesin-dependent pathway, distinct from the ZEB1-E-cadherin axis, through which miR-200 can regulate tumour cell plasticity and metastasis.

Indexed as

Neoplasm InvasivenessSignal TransductionAnimalsBreast NeoplasmsCadherinsCell Line, TumorFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHomeodomain ProteinsHumansLung NeoplasmsMammary Neoplasms, ExperimentalMiceMicrofilament ProteinsMicroRNAsCadherinsHomeodomain ProteinsMicrofilament ProteinsMicroRNAsMIRN200 microRNA, humanmoesinRepressor ProteinsTranscription FactorsZEB1 protein, humanZEB2 protein, humanZinc Finger E-box-Binding Homeobox 1Zinc Finger E-box Binding Homeobox 2

Identifiers

PMID24037528
OpenAlexW2092691314

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.