Evidence map›Paper›PMID 28629477›Full record

ArticleCell communication and signaling : CCS2017

Identification of EGF-NF-κB-FOXC1 signaling axis in basal-like breast cancer.

Stacey Chung, Yanli Jin, Bingchen Han, Ying Qu, Bowen Gao, Armando E Giuliano, Xiaojiang Cui

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

27 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Telomere Maintenance and Oncogenesis.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Review
  7. The Role of the Fox Gene in Breast Cancer Progression.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. The circular RNA circCPE regulates myoblast development by sponging miR-138.Journal of animal science and biotechnology · 2021
    Article
  14. Article
  15. Article
  16. Review
  17. Article
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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

7 authors at 1 institution in 1 country.

Stacey ChungDepartment of Surgery, Samuel Oschin Cancer Institute, Cedars-Sinai Medical Center, California, Los Angeles, 90048, USA.
Yanli JinDepartment of Surgery, Samuel Oschin Cancer Institute, Cedars-Sinai Medical Center, California, Los Angeles, 90048, USA.
Bingchen HanDepartment of Surgery, Samuel Oschin Cancer Institute, Cedars-Sinai Medical Center, California, Los Angeles, 90048, USA.
Ying QuDepartment of Surgery, Samuel Oschin Cancer Institute, Cedars-Sinai Medical Center, California, Los Angeles, 90048, USA.
Bowen GaoDepartment of Surgery, Samuel Oschin Cancer Institute, Cedars-Sinai Medical Center, California, Los Angeles, 90048, USA.
Armando E GiulianoDepartment of Surgery, Samuel Oschin Cancer Institute, Cedars-Sinai Medical Center, California, Los Angeles, 90048, USA.
Xiaojiang CuiDepartment of Surgery, Samuel Oschin Cancer Institute, Cedars-Sinai Medical Center, California, Los Angeles, 90048, USA. xiaojiang.cui@cshs.org.
Cedars-Sinai Medical Center · US

Funding

The Role of FOXCI in Basal-like Breast CancerR01CA151610 · NCI · SAINT JOHN'S CANCER INSTITUTE · PI CUI, XIAOJIANG · 2011 to 2022
$3.8M
NCI NIH HHS R01 CA151610
6 · The paper itself

Abstract

backgroundThe pathogenesis of human basal-like breast cancer (BLBC) is not well understood and patients with BLBC have a poor prognosis. Expression of the epidermal growth factor receptor (EGFR) and nuclear factor-κB (NF-κB) is well-known to be upregulated in BLBC. The forkhead box C1 (FOXC1) transcription factor, an important prognostic biomarker specific for BLBC, has been shown to be induced by EGF and is critical for EGF effects in breast cancer cells. How FOXC1 is transcriptionally activated in BLBC is not clear.

methodsLuciferase reporter assays were performed to show that NF-κB-p65 enhances FOXC1 promoter activity in BLBC cells (MDA-MB-468). Electrophoretic mobility shift assay, biotinylated oligonucleotide precipitation assay, and chromatin immunoprecipitation assay were used to show that NF-κB interacts and binds to the promoter region of FOXC1.

resultsIn this study, we demonstrate that NF-κB is a pivotal mediator of the EGF/EGFR regulation of FOXC1 expression by binding to the FOXC1 promoter to activate FOXC1 transcription. Loss or inhibition of NF-κB diminished FOXC1 expression.

conclusionCollectively, our findings reveal a novel EGFR-NF-κB-FOXC1 signaling axis that is critical for BLBC cell function, supporting the notion that intervention in the FOXC1 pathway may provide potential modalities for BLBC treatment.

Indexed as

Signal TransductionBase SequenceBreast NeoplasmsCell Line, TumorEpidermal Growth FactorForkhead Transcription FactorsHumansNF-kappa BPromoter Regions, GeneticEpidermal Growth FactorForkhead Transcription FactorsFOXC1 protein, humanNF-kappa BBasal-like breast cancerEpidermal growth factorFOXC1NF-κB

Identifiers

PMID28629477
PMCPMC5477115
OpenAlexW2650499366

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.