Evidence map›Paper›PMID 33417085›Full record

ArticleBreast cancer research and treatment2021

FOXA1 is a determinant of drug resistance in breast cancer cells.

Uttom Kumar, Anastasia Ardasheva, Zimam Mahmud, R Charles Coombes, Ernesto Yagüe

Open access · hybridAbstract read
In one paragraph

Article in Breast cancer research and treatment, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The Role of the Fox Gene in Breast Cancer Progression.International journal of molecular sciences · 2025
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  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

5 authors at 2 institutions in 2 countries.

Uttom KumarDivision of Cancer, Imperial College Faculty of Medicine, Hammersmith Hospital Campus, Du Cane Road, London, W12 0NN, UK.
Anastasia ArdashevaDivision of Cancer, Imperial College Faculty of Medicine, Hammersmith Hospital Campus, Du Cane Road, London, W12 0NN, UK.
Zimam MahmudDivision of Cancer, Imperial College Faculty of Medicine, Hammersmith Hospital Campus, Du Cane Road, London, W12 0NN, UK.
R Charles CoombesDivision of Cancer, Imperial College Faculty of Medicine, Hammersmith Hospital Campus, Du Cane Road, London, W12 0NN, UK.
Ernesto YagüeDivision of Cancer, Imperial College Faculty of Medicine, Hammersmith Hospital Campus, Du Cane Road, London, W12 0NN, UK. ernesto.yague@imperial.ac.uk.ORCID http://orcid.org/0000-0003-2371-0032
Hammersmith Hospital · GBUniversity of Dhaka · BD

Funding

Cancer Research UK 12011Cancer Research UK 18784
6 · The paper itself

Abstract

purposeBreast cancer is one of the most commonly diagnosed cancers in women. Five subtypes of breast cancer differ in their genetic expression profiles and carry different prognostic values, with no treatments available for some types, such as triple-negative, due to the absence of genetic signatures that could otherwise be targeted by molecular therapies. Although endocrine treatments are largely successful for estrogen receptor (ER)-positive cancers, a significant proportion of patients with metastatic tumors fail to respond and acquire resistance to therapy. FOXA1 overexpression mediates endocrine therapy resistance in ER-positive breast cancer, although the regulation of chemotherapy response by FOXA1 has not been addressed previously. FOXA1, together with EP300 and RUNX1, regulates the expression of E-cadherin, and is expressed in luminal, but absent in triple-negative and basal-like breast cancers. We have previously determined that EP300 regulates drug resistance and tumor initiation capabilities in breast cancer cells.

methodsHere we describe the generation of breast cancer cell models in which FOXA1 expression has been modulated either by expression of hairpins targeting FOXA1 mRNA or overexpression plasmids.

resultsUpon FOXA1 knockdown in luminal MCF-7 and T47D cells, we found an increase in doxorubicin and paclitaxel sensitivity as well as a decrease in anchorage independence. Conversely, upregulation of FOXA1 in basal-like MDA-MB-231 cells led to an increase in drug resistance and anchorage independence.

conclusionTogether, these data suggest that FOXA1 plays a role in making tumors more aggressive.

Indexed as

Breast NeoplasmsBreastDrug ResistanceFemaleGene Expression Regulation, NeoplasticHepatocyte Nuclear Factor 3-alphaHumansFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphaAnchorage independenceBreast cancerE-cadherinFOXA1Multidrug resistance

Identifiers

PMID33417085
PMCPMC7990828
OpenAlexW3119904495

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.