Evidence map›Paper›PMID 27035620›Full record

ArticleCell death and differentiation2016

Restraining FOXO3-dependent transcriptional BMF activation underpins tumour growth and metastasis of E-cadherin-negative breast cancer.

M Hornsveld, M Tenhagen, R A van de Ven, A M M Smits, M H van Triest, M van Amersfoort, D E A Kloet, T B Dansen, B M Burgering, P W B Derksen

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 59 citations in OpenAlex.

  1. Toward targeted therapeutics for lobular breast cancer.The Journal of clinical investigation · 2026
    Review
  2. Article
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  7. The Role of the Fox Gene in Breast Cancer Progression.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Review
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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

10 authors at 1 institution in 1 country.

M HornsveldDepartment of Molecular Cancer Research, University Medical Center Utrecht, Utrecht, The Netherlands.
M TenhagenDepartment of Pathology, University Medical Center Utrecht, Utrecht, The Netherlands.
R A van de VenDepartment of Pathology, University Medical Center Utrecht, Utrecht, The Netherlands.
A M M SmitsDepartment of Molecular Cancer Research, University Medical Center Utrecht, Utrecht, The Netherlands.
M H van TriestDepartment of Molecular Cancer Research, University Medical Center Utrecht, Utrecht, The Netherlands.
M van AmersfoortDepartment of Pathology, University Medical Center Utrecht, Utrecht, The Netherlands.
D E A KloetDepartment of Molecular Cancer Research, University Medical Center Utrecht, Utrecht, The Netherlands.
T B DansenDepartment of Molecular Cancer Research, University Medical Center Utrecht, Utrecht, The Netherlands.
B M BurgeringDepartment of Molecular Cancer Research, University Medical Center Utrecht, Utrecht, The Netherlands.
P W B DerksenDepartment of Pathology, University Medical Center Utrecht, Utrecht, The Netherlands.
University Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of cellular adhesion leads to the progression of breast cancer through acquisition of anchorage independence, also known as resistance to anoikis. Although inactivation of E-cadherin is essential for acquisition of anoikis resistance, it has remained unclear how metastatic breast cancer cells counterbalance the induction of apoptosis without E-cadherin-dependent cellular adhesion. We report here that E-cadherin inactivation in breast cancer cells induces PI3K/AKT-dependent FOXO3 inhibition and identify FOXO3 as a novel and direct transcriptional activator of the pro-apoptotic protein BMF. As a result, E-cadherin-negative breast fail to upregulate BMF upon transfer to anchorage independence, leading to anoikis resistance. Conversely, expression of BMF in E-cadherin-negative metastatic breast cancer cells is sufficient to inhibit tumour growth and dissemination in mice. In conclusion, we have identified repression of BMF as a major cue that underpins anoikis resistance and tumour dissemination in E-cadherin-deficient metastatic breast cancer.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAnoikisApoptosisBcl-2-Like Protein 11Breast NeoplasmsCadherinsCell Line, TumorDoxycyclineFemaleForkhead Box Protein O3HumansLung NeoplasmsMCF-7 CellsMicePhosphatidylinositol 3-KinasesAdaptor Proteins, Signal TransducingBcl-2-Like Protein 11Bmf protein, mouseCadherinsDoxycyclineForkhead Box Protein O3Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID27035620
PMCPMC5072425
OpenAlexW2325641180

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.