Evidence map›Paper›PMID 27377963›Full record

ArticleCellular signalling2016

The dual role of FOXF2 in regulation of DNA replication and the epithelial-mesenchymal transition in breast cancer progression.

Pang-Kuo Lo, Ji Shin Lee, Xiaohui Liang, Saraswati Sukumar

Open access · greenAbstract read
In one paragraph

Article in Cellular signalling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. The Role of the Fox Gene in Breast Cancer Progression.International journal of molecular sciences · 2025
    Review
  2. Review
  3. Translational cancer research · 2024
    Article
  4. Article
  5. Article
  6. Characterization of the skin keloid microenvironment.Cell communication and signaling : CCS · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Breast cancer (Dove Medical Press) · 2021
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Pan-cancer survey of epithelial-mesenchymal transition markers across the Cancer Genome Atlas.Developmental dynamics : an official publication of the American Association of Anatomists · 2018
    Article
  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

4 authors at 2 institutions in 1 country.

Pang-Kuo LoBreast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: PLo@som.umaryland.edu.
Ji Shin LeeBreast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Xiaohui LiangBreast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Saraswati SukumarBreast Cancer Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: saras@jhmi.edu.
Johns Hopkins University · USSidney Kimmel Comprehensive Cancer Center · US

Funding

VACCINES--A NEW PARADIGM FOR BREAST CANCERP50CA088843 · NCI · JOHNS HOPKINS UNIVERSITY · PI DAVIDSON, NANCY ELLEN · 2000 to 2010
$27.8M
NCI NIH HHS P50 CA088843
6 · The paper itself

Abstract

Dysregulation of Forkhead-box (FOX) transcription factors is linked to cancers of numerous tissue types. Here, we report that FOXF2 is frequently silenced in luminal-type and HER2-positive breast cancers, but is overexpressed in basal-like breast cancers; thus, FOXF2 appears to play distinct roles in different breast cancer subtypes. Inactivation of FOXF2 in luminal-type and HER2-positive breast cancers is attributable to epigenetic silencing. Silencing of FOXF2 is associated with poor prognosis in luminal-type breast cancer. Ectopic expression of FOXF2 in luminal and HER2-positive breast cancer cells suppresses their tumorigenic properties in vitro and in vivo via inhibition of the CDK2-RB-E2F cascade. The in vivo function of FOXF2 is to maintain the stringency of DNA replication, and its loss triggers dysregulation of DNA replication, which in turn activates the p53 checkpoint pathway. Besides its role in cell cycle regulation, FOXF2 is functionally required for mobility and epithelial-to-mesenchymal transition (EMT) of normal breast epithelial cells. In basal-like breast cancer cells, the cell-cycle function of FOXF2 is impaired. However, the EMT function of FOXF2 is still required for mobility, invasiveness and anchorage-independent growth of basal-like breast cancer cells. Our gene expression profiling studies demonstrate that FOXF2 regulates the expression of genes implicated in cell cycle and EMT regulation. Moreover, FOXF2 is highly co-expressed with basal- and metastasis-related genes in breast cancer. These findings suggest that FOXF2 has a dual role in breast tumorigenesis and functions as either a tumor suppressor or an oncogene depending on the breast tumor subtype.

Indexed as

Disease ProgressionGene Expression Regulation, NeoplasticAnimalsBreast NeoplasmsCarcinogenesisCell CycleCell Line, TumorCell ProliferationDNA ReplicationEpigenesis, GeneticEpithelial-Mesenchymal TransitionErb-b2 Receptor Tyrosine KinasesFemaleForkhead Transcription FactorsGene SilencingHumansERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesForkhead Transcription FactorsFOXF2 protein, humanBasal-like/triple-negative breast cancerDNA methylationEpithelial-to-mesenchymal transitionFOXF2HER2-positive breast cancerLuminal breast cancer

Identifiers

PMID27377963
PMCPMC5056599
OpenAlexW2463431879

What OpenQuestion holds

Textmetadata
LicenceTDM
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.