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Targeting EZH2 reactivates a breast cancer subtype-specific anti-metastatic transcriptional program driven by FOXC1.
This study demonstrates that FOXC1 induces cancer stem cells (CSCs)-like properties in non-small cell lung cancer (NSCLC) by promoting beta-catenin expression. The findings indicate that FOXC1 is a potential molecular target for anti-CSC-based therapies in NSCLC
Foxc1 promoted cell proliferation by upregulation PI3K/AKT signaling, which was inflammation-dependent.
Knockdown of FOXC1 markedly suppressed cell migration and invasion in vitro, and resulted in downregulation of phosphorylatedRACalpha serine/threonineprotein kinase, protooncogene cMyc and Bcell lymphoma 2.
Results provide evidence that FOXC1 is not required for initiation of EMT events but rather participates in the specification of mesenchymal cell phenotype through regulation of FGF receptor switching from FGFR2-IIIb to FGFR1-IIIc in response to TGFb1-induced EMT.
In regulating cervical cancers metastasis by targeting FOXC1.
Forkhead box C1 protein (FOXC1) promotes melanoma cell function by regulating macrophage stimulating 1 receptor (MST1R) and activating MST1R/PI3K/AKT pathway.
expression of FOXC1 in BRCA1 mutant cell lines correlates with sensitivity to olaparib. Whether this is due to rates of proliferation or another mechanism is yet to be explored, but this, and the specificity of FOXC1 in BRCA1-mutant tumors, suggests a possible role for FOXC1 as a marker for targeted therapy.
novel EGFR-NF-kappaB-FOXC1 signaling axis that is critical for BLBC cell function
Taken together, these data indicate that FOXC1 is a novel hypoxia-induced transcription factor and plays a critical role in tumor microenvironment-promoted lung cancer progression.
Genomic analysis of blood and excised valve tissue showed down-regulation of FOXC1 but also FOXC2 expression in the diseased aortic valve. This allows us to speculate on the potential role of FOXC1 in aortic valve anomalies.
Results showed a significant higher FOXC1 expression in estrogen receptor-negative breast cancer than that in estrogen receptor-positive. Its overexpression reduced expression of ERalpha and cellular responses to tamoxifen suggesting that FOXC1 regulated expression of ERalpha and affected sensitivity of tamoxifen treatment in breast cancer
present work reveals that FOXC1 is an important regulator of exocytosis and establishes a new link between FOXC1 and MYOC-associated glaucoma
Glaucoma prevalence and phenotype are characterized in a cohort of glaucoma patients and their family members with FOXC1 variants.
FOXC1 and FOXC2 are essential regulators of lymphangiogenesis and may have roles in lymphatic-associated diseases
This review will summarize current knowledge on the function and regulation of FOXC1 in tumor development and progression with a focus on basal-like breast cancer, as well as the implications of these new findings in cancer diagnosis and treatment. [review]
Here, we demonstrate a novel FOXC1-driven mechanism that suppresses ERa expression in breast cancer. We find that FOXC1 competes with GATA-binding protein 3 (GATA3) for the same binding regions in the cis-regulatory elements upstream of the ERa gene and thereby downregulates ERa expression and consequently its transcriptional activity
A novel heterozygous FOXC1 variant segregated with the disease in a family with Axenfeld Rieger Syndrome. A novel homozygous variant in the FOXC1 gene segregated in a family with ARS and congenital glaucoma.
Our findings suggested that FOXCUT expression contributed to the development and progression of nasopharyngeal carcinoma by targeting FOXC1 and that FOXCUT might be useful as a potential nasopharyngeal carcinoma biomarker and therapeutic target.
this study defines FOXC1 as a regulator specific for KC terminal differentiation and establishes its potential position in the genetic regulatory network.
These findings suggest that Foxc1 is an important regulator to further chondrogenesis and initiate the ossification of the presphenoid and basisphenoid bones.
Lineage tracing experiments in Foxc1 mutant mouse cerebella indicate that aberrant migration of granule cell progenitors destined to form the posterior-most lobule causes this cerebellar malformation phenotype.
Foxc1 regulates both early cardiomyogenesis and the functional properties of embryonic stem cell-derived cardiomyocytes.
These data indicate that Foxc1 expression is regulated by BMP4 and FOXC1 functions in the commitment of progenitor cells to the osteoblast fate and its expression is reduced when differentiation proceeds.
Foxc1 regulates sweat duct luminal cell differentiation and mimic apocrine miliaria.
Compound, NC-specific Foxc1; Foxc2 homozygous mutant mice have more severe defects in structures of the ocular surface, such as the cornea and eyelids, accompanied by significant declines in the expression of another key developmental factor, Pitx2, and its downstream effector Dkk2, which antagonizes canonical Wnt signaling.
These findings offer the first evidence for a role of the meninges in brain vascular development and provide new insight into potential causes of cerebrovascular defects in patients with FOXC1 mutations.
Foxc1 and Foxc2 maintain glomerular podocyte integrity by regulating the gene expression.
Foxc1 and Foxc2 have a role in kidney and axial skeleton development.
FOXC1 maintains the hair follicle stem cell niche and governs stem cell quiescence to preserve long-term tissue-regenerating potential.FOXC1 is necessary to establish a multiple-bulge hair follicle architecture.
deletion of Foxc1 and Foxc2 specifically in Pax3-positive cells affects cell fate choices in the dermomyotome of somites at forelimb level, promoting the myogenic cell fate at the expense of endothelial cells that migrate to the limb
Foxc1 is an important transcriptional partner of Ihh-Gli2 signalling during endochondral ossification, and that disruption of the Foxc1-Gli2 interaction causes skeletal abnormalities observed in the Axenfeld-Rieger syndrome.
In self-renewing stem cells (SCs), Foxc1 activates Nfatc1 and bone morphogenetic protein (BMP) signaling, two key mechanisms that govern quiescence. These findings reveal a dynamic, cell-intrinsic mechanism used by hair follicle SCs to reinforce quiescence upon self-renewal and suggest a unique ability of SCs to maintain cell identity.
These observations reveal an essential role for Foxc1 in the early stage of vascular formation in the telencephalon.
loss of Foxc1 non-autonomously induces a rapid and devastating decrease in embryonic cerebellar ventricular zone radial glial proliferation and concurrent increase in cerebellar neuronal differentiation
A loss of Foxc1 function affects skull bone formation of the apical region.
Together our data demonstrates that Foxc1 - Fgf8 signaling regulates mammalian jaw patterning and provides a mechanistic basis for the pathogenesis of syngnathia.
identification of Foxc1 as a specific transcriptional regulator essential for development and maintenance of the mesenchymal niches for haematopoietic stem and progenitor cells
Identify mesodermal foxc1a/b as a direct upstream regulator of etsrp in angioblasts. This establishes a new molecular link in the process of mesoderm specification into angioblast.
This study reveals an important role for FOXC1 in the direct regulation of the FGF19-FGFR4-MAPK pathway to promote both the development and maintenance of anterior segment structures within the eye.
This gene belongs to the forkhead family of transcription factors which is characterized by a distinct DNA-binding forkhead domain. The specific function of this gene has not yet been determined\; however, it has been shown to play a role in the regulation of embryonic and ocular development. Mutations in this gene cause various glaucoma phenotypes including primary congenital glaucoma, autosomal dominant iridogoniodysgenesis anomaly, and Axenfeld-Rieger anomaly.
forkhead box protein C1
, forkhead, drosophila, homolog-like 7
, forkhead-related activator 3
, forkhead-related protein FKHL7
, forkhead-related transcription factor 3
, forkhead/winged helix-like transcription factor 7
, myeloid factor-delta
, forkhead box C1
, forkhead box protein C1-B
, Forkhead box protein C1
, congenital hydrocephalus
, mesoderm/mesenchyme forkhead 1
, transcription factor FKH-1
, winged helix protein CWH-6
, winged-helix transcription factor
, forkhead box C1-B