ArticlePRAS open2017
The controversial role of forkhead box F2 (FOXF2) transcription factor in breast cancer.
Article in PRAS open, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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.
Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Characterization of the skin keloid microenvironment.Cell communication and signaling : CCS · 2023Review
- Unraveling the Molecular Puzzle: Exploring Gene Networks across Diverse EMT Status of Cell Lines.International journal of molecular sciences · 2023Review
- Global gene network exploration based on explainable artificial intelligence approach.PloS one · 2020Article
- Foxf2 plays a dual role during transforming growth factor beta-induced epithelial to mesenchymal transition by promoting apoptosis yet enabling cell junction dissolution and migration.Breast cancer research : BCR · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Deregulating the subcellular localization, functions and expression of Forkhead box (FOX) transcription factors that are critically involved in embryonic development and multiple biological processes is known to result in the development and progression of diseases, in particular cancer. Human FOXF transcription factors, including FOXF1 and FOXF2, are a subfamily of the FOX gene family. The recent findings from ours and others have linked FOXF2 to breast cancer development and progression. Our studies have shown that FOXF2 acts as a tumor-suppressive inhibitor of DNA replication in luminal and HER2-positive breast cancers and as an oncogenic activator of the epithelial-mesenchymal transition (EMT) in triple-negative/basal-like breast cancers (TN/BLBC), suggesting that FOXF2 plays a dual role in breast cancer. However, studies from Feng's research group have pointed out an opposite role of FOXF2 in TN/BLBC, which acts as an inhibitor of the EMT and as a promoter of cell proliferation in TN/BLBC. These discrepancies between our and Feng's studies have caused controversy in the role of FOXF2 in breast cancer. This article reviews both studies and discusses what causes might have led to these inconsistencies as well as what future experiments are needed to solve this debate.
Indexed as
Identifiers
29046905PMC5642972W2974033775What OpenQuestion holds
Registered trials
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.