Affinage

FOXN3

Forkhead box protein N3 · UniProt O00409

Length
490 aa
Mass
53.8 kDa
Annotated
2026-06-09
47 papers in source corpus 25 papers cited in narrative 25 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FOXN3 (CHES1) is a forkhead-family transcriptional repressor that constrains proliferative, metastatic, fibrotic, metabolic, and ciliogenic gene programs across multiple tissues by binding promoters directly and recruiting corepressor machinery (PMID:30826165, PMID:28805661, PMID:40663603). Its DNA-binding domain achieves bispecific recognition, engaging both the canonical forkhead (FKH) motif and the distinct FHL motif using the same residues but exploiting differences in DNA shape between the two complexes (PMID:30826165). FOXN3 represses transcription as a component of the SIN3A/HDAC1/HDAC2 corepressor complex, and in estrogen receptor-positive breast cancer the estrogen-induced lncRNA NEAT1 bridges FOXN3 to SIN3A to silence EMT genes such as GATA3 and transrepress ERα itself (PMID:28805661, PMID:16951149). It directly binds and represses an array of target promoters that link it to growth control—PIM2 (gating protein synthesis via 4EBP1), E2F5, SIRT6, RPS15A, EP300, and the MYC locus governing hepatic glucose metabolism (PMID:24403608, PMID:27259277, PMID:30483801, PMID:37016167, PMID:39607349, PMID:27292639). FOXN3 activity is set by phosphorylation-coupled degradation: p38 phosphorylates S83/S85 to drive its proteasomal turnover and license NF-κB activation, while NEK6 phosphorylates S412/S416 to destabilize it and release Smad2/3/4-driven pro-fibrotic transcription; PARP1 opposes the p38 axis to stabilize FOXN3 and suppress fibrosis (PMID:36794705, PMID:39984467, PMID:41481720). In developing retina, FOXN3 enforces neuronal identity by repressing ciliary genes and their transactivators Foxj1 and Rfx family members, partnering with Rfx3 through a conserved LXXLXWL hydrophobic motif (PMID:40663603, PMID:41766387).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2005 Medium

    Establishing that FOXN3 acts as a transcriptional repressor and identifying its corepressor contacts was the first step in defining its molecular function.

    Evidence Reporter gene assay with heterologous DNA-binding fusion plus cytoplasmic two-hybrid and co-IP identifying SKIP interaction

    PMID:16102918

    Open questions at the time
    • Did not identify direct genomic targets
    • Functional consequence of SKIP binding on endogenous genes untested
  2. 2006 High

    Linking FOXN3 to menin and the mSin3a/HDAC complex placed it in a DNA-damage S-phase checkpoint and explained how it represses transcription.

    Evidence Drosophila genetic screen with radiation-induced checkpoint assays plus reciprocal co-IP in human cells

    PMID:16951149

    Open questions at the time
    • Direct checkpoint target genes not defined
    • Whether menin interaction operates outside DNA damage unclear
  3. 2010 Medium

    A loss-of-function mouse revealed an essential developmental role for FOXN3 in craniofacial and osteogenic gene programs.

    Evidence Foxn3 mutant mouse phenotyping with osteogenic gene expression analysis

    PMID:20691664

    Open questions at the time
    • Direct target promoters in craniofacial tissue not identified
    • Corepressor dependence in this context untested
  4. 2014 Medium

    Demonstrating direct PIM2 promoter binding connected FOXN3 repression to control of protein synthesis and proliferation.

    Evidence ChIP, shRNA/overexpression, domain mutants, and 4EBP1 phosphorylation analysis with PIM2/eIF4E rescue

    PMID:24403608

    Open questions at the time
    • Single tumor cell context
    • Whether SIN3A complex is required for PIM2 repression untested
  5. 2016 Medium

    Multiple studies established FOXN3 as a tumor-suppressive repressor of proliferation genes (E2F5) and as a metabolic regulator repressing MYC to control hepatic gluconeogenesis.

    Evidence Promoter-reporter/xenograft for E2F5 in HCC; transgenic zebrafish overexpression with ChIP at MYC locus and glucose phenotyping

    PMID:27259277 PMID:27292639

    Open questions at the time
    • Cofactor requirements for these promoters not defined
    • Cross-tissue generality of MYC repression unestablished
  6. 2017 High

    Identification of the NEAT1-dependent FOXN3-SIN3A complex showed how a lncRNA reprograms FOXN3 into an EMT/metastasis driver in breast cancer, and a separate study showed FOXN3 blocks β-catenin/TCF signaling.

    Evidence RIP-Seq, ChIP-Seq, Co-IP, invasion/metastasis assays (NEAT1); Co-IP and reporter assays for β-catenin–TCF4 disruption

    PMID:28039460 PMID:28805661

    Open questions at the time
    • How NEAT1 selectively licenses FOXN3-SIN3A binding mechanistically unresolved
    • Context-dependence of pro- vs anti-tumor roles unexplained
  7. 2019 High

    Co-crystal structures resolved how FOXN3 reads two unrelated DNA motifs, defining the structural basis of its bispecific recognition.

    Evidence X-ray co-crystal structures of the FoxN3 DBD bound to FKH and FHL sites

    PMID:30826165

    Open questions at the time
    • Genome-wide partition of FKH vs FHL site usage in vivo unknown
    • Whether motif choice dictates distinct target programs untested
  8. 2019 Medium

    Liver-specific knockdown defined FOXN3 as a regulator of gluconeogenic substrate selection beyond glucagon and insulin.

    Evidence AAV8-shRNA liver knockdown in mice with dynamic glucose, pyruvate, and glutamine challenges

    PMID:31552709

    Open questions at the time
    • Direct promoter targets of amino acid handling genes not shown
    • Mechanism distinguishing substrate classes unresolved
  9. 2023 High

    Mapping S83/S85 phosphorylation revealed a p38-driven degradation switch coupling FOXN3 turnover to NF-κB activation in inflammation.

    Evidence In vitro kinase assays, S83A/S85A mutagenesis, hnRNPU/IκBα competition Co-IP, and phospho-ablation mouse models

    PMID:36794705

    Open questions at the time
    • Whether the hnRNPU competition mechanism operates outside lung inflammation untested
    • Upstream activators of p38 in this circuit not defined
  10. 2025 High

    A second phospho-degradation axis (NEK6 at S412/S416) was shown to release Smad-driven fibrotic transcription, and FOXN3 was defined as a facilitator of Smad4 ubiquitination.

    Evidence Kinase assays, S412/S416 mutagenesis, ChIP, ubiquitination assays, conditional overexpression in vivo, and clinical tissue analysis

    PMID:39984467

    Open questions at the time
    • How FOXN3 promotes β-TrCP-mediated Smad4 ubiquitination structurally unresolved
    • Relationship between the NEK6 and p38 phospho-sites unclear
  11. 2025 High

    Conditional knockout revealed FOXN3 as a repressor of ciliary gene programs required for nonphotoreceptor retinal neuron identity and function.

    Evidence Retina-specific conditional KO, ERG, scRNA-seq, CUT&RUN, and transcription assays showing direct repression of ciliary genes and Foxj1/Rfx transactivators

    PMID:40663603

    Open questions at the time
    • Corepressor complex used at ciliary promoters not defined
    • Whether this repression extends beyond retina untested
  12. 2026 High

    The PARP1-FOXN3-p38-Smad feedback loop and the LXXLXWL-mediated FOXN3-Rfx3 interaction defined how FOXN3 stability is controlled and how it physically docks its corepressive partner.

    Evidence Lung-specific PARP1 KO with FOXN3 rescue, Co-IP and ChIP (fibrosis circuit); LXXLXWL motif mutagenesis, Co-IP, CUT&RUN, and AlphaFold 3 prediction (Rfx3 interaction)

    PMID:41481720 PMID:41766387

    Open questions at the time
    • Direct biochemical mechanism by which PARP1 blocks p38 phosphorylation not resolved
    • Structural validation of the FOXN3-Rfx3 interface beyond prediction lacking

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how FOXN3's bispecific DNA recognition, corepressor choice (SIN3A vs Rfx3), and phospho-degradation inputs are integrated to select tissue-specific target programs.
  • No unified model linking motif usage to context-specific repertoires
  • Determinants of pro- vs anti-tumor outcomes unknown
  • Genome-wide cofactor partitioning across tissues uncharacterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 4 GO:0140110 transcription regulator activity 4 GO:0098772 molecular function regulator activity 3
Localization
GO:0005634 nucleus 2
Pathway
R-HSA-1430728 Metabolism 3 R-HSA-162582 Signal Transduction 3 R-HSA-74160 Gene expression (Transcription) 3
Partners
CTNNB1HNRNPUMEN1NEAT1NEK6PARP1RFX3SIN3A
Complex memberships
FOXN3-NEAT1-SIN3A complexSIN3A/HDAC1/HDAC2 corepressor complex

Evidence

Reading pass · 25 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2019 Co-crystal structures of the FoxN3 DNA-binding domain bound to both the canonical forkhead (FKH) motif (RYAAAYA) and the distinct FHL motif (GACGC) revealed that FoxN3 adopts a similar protein conformation to recognize both motifs using the same amino acids, but the DNA shape (structure) differs between the two complexes, explaining bispecific DNA recognition. Co-crystal structures (X-ray crystallography) of FoxN3 DBD bound to FKH and FHL DNA sites Molecular cell High 30826165
2017 FOXN3 is a transcriptional repressor physically associated with the SIN3A repressor complex in estrogen receptor-positive breast cancer cells. The long noncoding RNA NEAT1, induced by estrogen, is required for FOXN3 interactions with the SIN3A complex. The FOXN3-NEAT1-SIN3A complex represses genes including GATA3 involved in EMT, promotes EMT and invasion in vitro and metastasis in vivo, and also transrepresses ERα itself forming a negative-feedback loop. RNA immunoprecipitation coupled to high-throughput sequencing (RIP-Seq), ChIP-Seq, co-immunoprecipitation, RNA-seq, in vitro invasion assays, in vivo metastasis models The Journal of clinical investigation High 28805661
2006 FOXN3 (CHES1) was identified as an interacting protein of menin (MEN1) by genetic screen in Drosophila; overexpression of CHES1 restored cell cycle arrest and viability of MEN1 mutant flies after ionizing radiation. A biochemical interaction between human menin and CHES1 was confirmed, requiring the COOH-terminus of menin (frequently mutated in MEN1 patients). CHES1 is a component of a transcriptional repressor complex including mSin3a, HDAC1, and HDAC2, and participates in an S-phase checkpoint pathway in DNA damage response. Drosophila genetic screen, co-immunoprecipitation in mammalian cells, cell viability and checkpoint assays in MEFs and Drosophila larval tissue Cancer research High 16951149
2005 The carboxyl terminus of CHES1 (FOXN3) fused to a heterologous DNA-binding domain represses reporter gene transcription. CHES1 interacts with Ski-interacting protein (SKIP/NCoA-62), a transcriptional co-regulator associated with repressor complexes, via a region within the final 66 hydrophobic residues of SKIP, defining a new protein-protein interaction domain of SKIP. Interaction was confirmed by co-immunoprecipitation in mammalian cells. Reporter gene transcription assay, cytoplasmic two-hybrid screen, co-immunoprecipitation in mammalian cells Gene Medium 16102918
2023 FOXN3 ameliorates MRSA-induced pulmonary inflammatory injury by inactivating NF-κB signaling. Mechanistically, FOXN3 competes with IκBα for binding to hnRNPU, blocking β-TrCP-mediated IκBα degradation and thus preventing NF-κB activation. p38 directly phosphorylates FOXN3 at S83 and S85, inducing its dissociation from hnRNPU, promoting NF-κB activation, and triggering proteasomal degradation of phosphorylated FOXN3. hnRNPU is essential for p38-mediated FOXN3 phosphorylation and subsequent degradation. In vitro phosphorylation assays, co-immunoprecipitation, site-directed mutagenesis (S83A/S85A), genetic ablation of FOXN3 phosphorylation in mouse models, proteasome inhibitor experiments Nucleic acids research High 36794705
2025 NEK6 phosphorylates FOXN3 at S412 and S416 in response to pro-fibrotic stimuli, leading to FOXN3 degradation. FOXN3 suppresses pulmonary fibrosis by inhibiting Smad transcriptional activity: it targets Smad response gene promoters and facilitates Smad4 ubiquitination, disrupting the Smad2/3/4 complex association with chromatin. Loss of FOXN3 (via NEK6 phosphorylation) inhibits β-TrCP-mediated ubiquitination of Smad4, stabilizing the Smad complex and promoting pro-fibrotic transcription. In vitro kinase assays, site-directed mutagenesis (S412/S416), ChIP assays, ubiquitination assays, co-immunoprecipitation, conditional FOXN3 overexpression in vivo, clinical tissue analysis Nature communications High 39984467
2026 PARP1 stabilizes FOXN3 by preventing its p38-mediated phosphorylation and subsequent degradation. Lung-specific knockout of PARP1 promotes pulmonary fibrosis by reducing FOXN3 abundance. Conditional overexpression of FOXN3 rescues fibrosis from PARP1 KO by impeding Smad signaling. p38 is itself a Smad response gene transcriptionally repressed by the PARP1/FOXN3 complex, establishing a feedback loop where loss of PARP1 or FOXN3 increases p38, which further degrades FOXN3 and activates Smad signaling. Lung-specific PARP1 knockout mice, conditional FOXN3 overexpression, co-immunoprecipitation, phosphorylation assays, ChIP, RNA-seq Science advances High 41481720
2014 CHES1 (FOXN3) decreases protein synthesis and cell proliferation in tumor cell lines in a manner dependent on its forkhead DNA-binding domain and nuclear localization. CHES1 directly binds the promoter of PIM2 and represses PIM2 expression; reduced PIM2 leads to decreased phosphorylation of the PIM2 target 4EBP1. Overexpression of PIM2 or eIF4E partially reverses the antiproliferative effect of CHES1, placing PIM2 and protein biosynthesis as key effectors. ChIP (direct promoter binding), shRNA knockdown, overexpression, domain mutant analysis, proliferation assays, 4EBP1 phosphorylation analysis Molecular biology of the cell Medium 24403608
2016 FOXN3 represses the promoter activity of E2F5 in hepatocellular carcinoma cells, reducing E2F5 mRNA and protein expression, and thereby inhibits HCC cell proliferation in vitro and in vivo. Promoter-reporter luciferase assay, qPCR, Western blot, in vitro proliferation assays, in vivo xenograft models Oncotarget Medium 27259277
2016 FOXN3 is a transcriptional repressor that regulates hepatic glucose metabolism. Overexpression of zebrafish foxn3 or human FOXN3 in zebrafish liver increases gluconeogenic gene expression, whole-larval free glucose, and adult fasting blood glucose while decreasing glycolytic gene expression. FOXN3 suppresses expression of MYC (mycb), a known regulator of glucose-utilization enzymes. Human FOXN3 was shown to bind DNA sequences in the human MYC and zebrafish mycb loci. Transgenic zebrafish overexpression, ChIP showing FOXN3 binding to MYC locus, glucose measurements, gene expression analysis in zebrafish and human hepatoma cells, human population genetics (SNP-expression correlation in primary hepatocytes) Cell reports Medium 27292639
2018 Liver FOXN3 and glucagon regulate each other reciprocally to control fasting glucose. Glucagon decreases liver Foxn3 protein and transcript levels in mice and zebrafish. Zebrafish foxn3 loss-of-function mutants have decreased fasting blood glucose, blood glucagon, liver gluconeogenic gene expression, and α cell mass. Liver-limited overexpression of foxn3 increases α cell mass, establishing a hepatocyte FOXN3-α cell glucagon axis. Zebrafish loss-of-function mutants, glucagon injection experiments, liver-limited transgenic overexpression, fasting glucose and glucagon measurements, oral glucose tolerance testing in human rs8004664 risk allele carriers Cell reports Medium 29996093
2019 Liver Foxn3 knockdown in mice (via AAV8-shRNA) decreases fasting glucose and increases Myc expression without altering fasting glucagon or insulin. Liver Foxn3 knockdown improves glucose tolerance, blunts pyruvate and glutamine tolerance, and modulates expression of amino acid transporters and catabolic enzymes, indicating FOXN3 regulates gluconeogenic substrate selection (particularly amino acid-based substrates) in the liver. AAV8-shRNA-mediated liver-specific Foxn3 knockdown in mice, dynamic metabolic tests (glucose tolerance, insulin tolerance, pyruvate challenge, glutamine challenge, glucagon challenge), gene expression analysis Physiological reports Medium 31552709
2017 FOXN3 binds to β-catenin and inhibits β-catenin/TCF signaling by blocking the interaction between β-catenin and TCF4 in colon cancer cells. Loss of FOXN3 activates β-catenin/TCF signaling and promotes growth, migration, and metastasis. Co-immunoprecipitation (FOXN3-β-catenin interaction), reporter assays (β-catenin/TCF transcriptional activity), forced expression and knockdown, in vitro growth/migration/invasion assays, in vivo metastasis model Oncotarget Medium 28039460
2010 Foxn3 is essential for craniofacial development in mice. Foxn3 mutant mice display partial embryonic and postnatal lethality, growth retardation, eye formation defects, dental anomalies, and craniofacial defects. Foxn3 mutant tissues are defective in expression of distinct osteogenic genes, implicating FOXN3 in transcriptional regulation during craniofacial development. Foxn3 mutant mouse model (loss-of-function), histological and phenotypic analysis, gene expression analysis of osteogenic genes Biochemical and biophysical research communications Medium 20691664
2022 Foxn3 mRNA is a direct target of miR-216b in the developing retina (identified by Argonaute PAR-CLIP and reporter analysis). Inhibition of Foxn3 by RNAi in the postnatal developing retina increased amacrine cell formation and reduced bipolar cell formation. Foxn3 disruption by CRISPR in embryonic retinal explants also increased amacrine cell formation, whereas Foxn3 overexpression inhibited amacrine cell formation prior to Ptf1a expression, establishing Foxn3 as a novel regulator of retinal interneuron fate. Argonaute PAR-CLIP, reporter assay, RNAi knockdown in postnatal retina, CRISPR disruption in retinal explants, cell-type quantification by immunostaining Development (Cambridge, England) Medium 34919141
2025 Foxn3 is a transcriptional repressor essential for suppressing ciliary gene expression in nonphotoreceptor retinal neurons. Retina-specific Foxn3 conditional knockout (Foxn3CKO) mice exhibit ectopic ciliary gene expression and abnormal ciliogenesis in bipolar and amacrine cells, reduced electroretinogram b-wave amplitudes, and displaced amacrine interneurons without affecting cell specification. CUT&RUN and transcription assays show that Foxn3 directly binds and represses promoters of ciliary genes and their transactivators Foxj1 and Rfx family members. Retina-specific conditional KO mice, electroretinography, single-cell RNA sequencing, CUT&RUN chromatin profiling, transcription assays, immunostaining Proceedings of the National Academy of Sciences of the United States of America High 40663603
2026 A short hydrophobic motif (LXXLXWL) shared by Foxn3, Foxn4, and Foxj1 is required for association of Foxn3 with Rfx3 and for transcriptional repression by Foxn3. AlphaFold 3 predicts this motif interacts with the Rfx3 dimerization domain; mutations in Rfx3 at the predicted interaction site disrupted Rfx3 association with Foxn3. Many upregulated ciliary genes in Foxn3-null retinas are bound by both Foxn3 and Rfx3 proteins. CUT&RUN, mutagenesis of the LXXLXWL motif, co-immunoprecipitation (Foxn3-Rfx3 interaction), AlphaFold 3 structural prediction, transcriptional reporter assays Development (Cambridge, England) High 41766387
2011 Overexpression of Ches1 (FOXN3) in oral cancer cells suppresses cell growth and arrests cells in the G2/M phase of the cell cycle. Overexpression in oral cancer cell lines, cell growth assay, flow cytometry cell cycle analysis Head & neck Low 20848451
2018 FOXN3 transcriptionally regulates SIRT6 in osteosarcoma cells, as shown by ChIP and luciferase reporter assay. FOXN3 also regulates MMP9 secretion via SIRT6, and suppresses proliferation, migration, and invasion of osteosarcoma cells. ChIP, quantitative ChIP, luciferase reporter assay, colony formation, wound healing, Transwell invasion assays Oncology reports Medium 30483801
2024 FOXN3 transcriptionally represses AKR1B10 in pancreatic cancer cells, as evidenced by label-free quantitative proteomics and functional rescue experiments showing AKR1B10 mediates FOXN3's effects on cellular senescence, proliferation, and invasion. Label-free quantitative proteomics, qPCR, Western blot, proliferation/invasion assays, cellular senescence assays, rescue experiments with AKR1B10 re-expression Biochimica et biophysica acta. Molecular basis of disease Low 38718846
2021 FOXN3 inhibits cell proliferation and invasion in glioma by inhibiting activation of the AKT/MDM2/p53 signaling pathway. FOXN3 overexpression decreased AKT/MDM2/p53 pathway activation, while FOXN3 knockdown facilitated its activation. qPCR, Western blot, CCK8, colony formation, flow cytometry, scratch wound, Transwell assays, in vivo xenograft, pathway activation analysis Aging Low 34511432
2023 FOXN3 directly binds to the promoter regions of RPS15A (at -1588/-1581 and -1476/-1467) and inhibits its transcriptional expression in ovarian cancer cells. Overexpression of RPS15A reverses FOXN3's inhibitory effects on ovarian cancer cell malignant behaviors. Dual-luciferase reporter assay, ChIP, overexpression/knockdown, proliferation, invasion, migration, angiogenesis assays, in vivo xenograft Human cell Medium 37016167
2024 FOXN3 transcriptionally inhibits EP300 expression in colorectal cancer cells by binding to the EP300 promoter. EP300 promotes H3K27ac enrichment at the SOX12 promoter, increasing SOX12 expression. Loss of FOXN3 thus indirectly enhances SOX12-driven cancer stemness and Wnt/β-catenin signaling. ChIP, dual luciferase reporter assays, overexpression/knockdown, sphere-forming assay, cell viability and invasion assays, in vivo tumor formation Molecular carcinogenesis Medium 39607349
2026 ChIP-seq identified E2F5 as a direct transcriptional target of FOXN3 in AML cells. FOXN3 overexpression decreases E2F5 mRNA and protein levels. E2F5 overexpression counteracts the proliferation-inhibitory effect of FOXN3. FOXN3 also modulates the MAPK signaling pathway and its downstream target EZH2. ChIP-seq, RT-qPCR, Western blot, luciferase reporter assay, RNA-seq, pathway enrichment analysis, co-transfection functional assays Blood and lymphatic cancer : targets and therapy Medium 41908971
2024 FOXN3 binds to the promoter region of FSIP1 (Fibrous Sheath Interacting Protein 1) in melanoma cells, regulating its expression. FOXN3 overexpression reduces autophagic activity in melanoma cells, and differential FOXN3 subcellular localization was observed between Vemurafenib-sensitive and -resistant melanoma cell lines. ChIP (FOXN3 binding to FSIP1 promoter), immunofluorescence (subcellular localization), colony formation, scratch wound healing, Transwell invasion assay, xenograft Clinical, cosmetic and investigational dermatology Low 39530064

Source papers

Stage 0 corpus · 47 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2017 The FOXN3-NEAT1-SIN3A repressor complex promotes progression of hormonally responsive breast cancer. The Journal of clinical investigation 170 28805661
2005 Identification of differentially expressed genes in oral squamous cell carcinoma (OSCC): overexpression of NPM, CDK1 and NDRG1 and underexpression of CHES1. International journal of cancer 85 15645429
2006 Multiple endocrine neoplasia type 1 interacts with forkhead transcription factor CHES1 in DNA damage response. Cancer research 67 16951149
2016 The transcription factor FOXN3 inhibits cell proliferation by downregulating E2F5 expression in hepatocellular carcinoma cells. Oncotarget 52 27259277
2014 Higher risk of aggressive pancreatic neuroendocrine tumors in MEN1 patients with MEN1 mutations affecting the CHES1 interacting MENIN domain. The Journal of clinical endocrinology and metabolism 52 25210877
2023 p38-mediated FOXN3 phosphorylation modulates lung inflammation and injury through the NF-κB signaling pathway. Nucleic acids research 47 36794705
2010 Foxn3 is essential for craniofacial development in mice and a putative candidate involved in human congenital craniofacial defects. Biochemical and biophysical research communications 45 20691664
2005 CHES1/FOXN3 interacts with Ski-interacting protein and acts as a transcriptional repressor. Gene 45 16102918
2019 Bispecific Forkhead Transcription Factor FoxN3 Recognizes Two Distinct Motifs with Different DNA Shapes. Molecular cell 43 30826165
2014 CHES1/FOXN3 regulates cell proliferation by repressing PIM2 and protein biosynthesis. Molecular biology of the cell 35 24403608
2017 Loss of FOXN3 in colon cancer activates beta-catenin/TCF signaling and promotes the growth and migration of cancer cells. Oncotarget 34 28039460
2016 FOXN3 Regulates Hepatic Glucose Utilization. Cell reports 32 27292639
2019 Recent Advances in Understanding FOXN3 in Breast Cancer, and Other Malignancies. Frontiers in oncology 28 31214487
2025 Phosphorylation of FOXN3 by NEK6 promotes pulmonary fibrosis through Smad signaling. Nature communications 27 39984467
2020 FOXN3 suppresses the growth and invasion of papillary thyroid cancer through the inactivation of Wnt/β-catenin pathway. Molecular and cellular endocrinology 23 32619584
2019 MicroRNA-378 regulates epithelial-mesenchymal transition and metastasis of melanoma by inhibiting FOXN3 expression through the Wnt/β-catenin pathway. Cell biology international 21 29972255
2011 Downregulation of Ches1 and other novel genes in oral cancer cells chronically exposed to areca nut extract. Head & neck 21 20848451
2020 MicroRNA-574-5p directly targets FOXN3 to mediate thyroid cancer progression via Wnt/β-catenin signaling pathway. Pathology, research and practice 17 32284251
2020 miR-574-5p Targets FOXN3 to Regulate the Invasion of Nasopharyngeal Carcinoma Cells via Wnt/β-Catenin Pathway. Technology in cancer research & treatment 15 33317407
2019 miR-611 promotes the proliferation, migration and invasion of tongue squamous cell carcinoma cells by targeting FOXN3. Oral diseases 15 31419344
2021 FOXN3 inhibits cell proliferation and invasion via modulating the AKT/MDM2/p53 axis in human glioma. Aging 14 34511432
2018 A Hepatocyte FOXN3-α Cell Glucagon Axis Regulates Fasting Glucose. Cell reports 13 29996093
2021 MicroRNA-182 promotes epithelial-mesenchymal transition by targeting FOXN3 in gallbladder cancer. Oncology letters 12 33574939
2019 Novel tumor-suppressor FOXN3 is downregulated in adult acute myeloid leukemia. Oncology letters 11 31423219
2019 FOXN3 controls liver glucose metabolism by regulating gluconeogenic substrate selection. Physiological reports 11 31552709
2018 FOXN3 is downregulated in osteosarcoma and transcriptionally regulates SIRT6, and suppresses migration and invasion in osteosarcoma. Oncology reports 11 30483801
2022 Regulation of retinal amacrine cell generation by miR-216b and Foxn3. Development (Cambridge, England) 9 34919141
2024 CHES1 modulated tumorigenesis and senescence of pancreas cancer cells through repressing AKR1B10. Biochimica et biophysica acta. Molecular basis of disease 8 38718846
2024 MiR-135b-5p promotes cetuximab resistance in colorectal cancer by regulating FOXN3. Cancer biology & therapy 7 38967961
2023 FOXN3 inhibits the progression of ovarian cancer through negatively regulating the expression of RPS15A. Human cell 6 37016167
2019 MicroRNA-378 promotes the malignant progression of oral squamous cell carcinoma by mediating FOXN3. European review for medical and pharmacological sciences 6 31364120
2021 Up-regulation of FOXN3-AS1 in invasive ductal carcinoma of breast cancer patients. Heliyon 5 34703931
2019 FoxN3 is necessary for the development of the interatrial septum, the ventricular trabeculae and the muscles at the head/trunk interface in the African clawed frog, Xenopus laevis (Lissamphibia: Anura: Pipidae). Developmental dynamics : an official publication of the American Association of Anatomists 5 30859697
2019 FOXN3 hyperglycemic risk allele and insulin sensitivity in humans. BMJ open diabetes research & care 5 31543974
2025 Foxn3 is required to suppress aberrant ciliogenesis in nonphotoreceptor retinal neurons. Proceedings of the National Academy of Sciences of the United States of America 4 40663603
2022 FOXN3 Expression Regulated by miR-299-5p Inhibiting the Proliferation, Migration and Invasion of Oral Squamous Cell Carcinoma Cells. Protein and peptide letters 4 35975858
2022 MAGI2-AS3 restrains proliferation, glycolysis, and triggers apoptosis in acute lymphoblastic leukemia via regulating miR-452-5p/FOXN3 pathway. Iranian journal of basic medical sciences 3 35656441
2025 Foxn3 is part of a transcriptional network that regulates primary cilia in the developing retina. bioRxiv : the preprint server for biology 2 39554069
2024 FOXN3 Downregulation in Colorectal Cancer Enhances Tumor Cell Stemness by Promoting EP300-Mediated Epigenetic Upregulation of SOX12. Molecular carcinogenesis 2 39607349
2026 Foxn3 is part of a transcriptional network that regulates primary cilia in the developing retina. Development (Cambridge, England) 1 41766387
2026 PARP1 stabilizes FOXN3 to suppress pulmonary fibrosis through p38-related feedback regulation. Science advances 0 41481720
2026 Crosstalk Between FOXN3 and E2F5 Reveals a Novel Tumor Suppressive Pathway in Acute Myeloid Leukemia via MAPK Signaling: Implications for Potential Future Targeted Therapy. Blood and lymphatic cancer : targets and therapy 0 41908971
2026 The exosomal miRNA/FOXN3 axis empowers fibroblasts with tumor-promoting functions via enhanced migration and altered secretome. Journal of nanobiotechnology 0 42249398
2025 Clinical significance of FOXN3 expression in Indian breast cancer patients. Scientific reports 0 40251258
2025 Cigarette smoking combines with genetic variants to regulate FOXN3 and associate with bladder cancer risk. Archives of toxicology 0 41361116
2024 Correlation between FOXN3-SIN3A complex expression in peripheral blood and non-syndromic cleft lip and palate in Xinjiang. Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology 0 39049650
2024 FOXN3 Regulates Autophagic Activity to Suppress Drug Resistance in Melanoma Cells. Clinical, cosmetic and investigational dermatology 0 39530064

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