Affinage

FNDC3B

Fibronectin type III domain-containing protein 3B · UniProt Q53EP0

Length
1204 aa
Mass
132.9 kDa
Annotated
2026-06-09
53 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FNDC3B (FAD104) is an ER/Golgi-anchored transmembrane protein that acts as a context-dependent regulator of cell differentiation, adhesion, and motility, with essential roles in mouse development (PMID:19138685, PMID:21704616). It is required postnatally, as gene disruption causes rapid neonatal death from lung dysplasia, reflecting a specific requirement for FNDC3B in the maturation of alveolar type II cells and surfactant protein expression (PMID:19138685, PMID:21704616). In mesenchymal lineage decisions FNDC3B promotes adipocyte differentiation while restraining osteoblast differentiation, the latter through its N-terminal proline-rich motif binding Smad1/5/8 and dampening their phosphorylation downstream of BMP signaling; its loss elevates Runx2 and causes craniosynostosis-like premature calvarial ossification (PMID:15527760, PMID:20493170, PMID:24052261). FNDC3B engages multiple partners through its N-terminal region to tune migration and epithelial-mesenchymal transition: it interacts with STAT3 to suppress STAT3 phosphorylation and metastatic behavior, cooperates with annexin A2 (ANXA2) to drive carcinoma migration, stabilizes MYH9 to activate Wnt/β-catenin signaling, and binds FAM83H to block its proteasomal degradation, promoting an EMT program (PMID:24052261, PMID:25671570, PMID:26948083, PMID:27385217, PMID:32232887, PMID:40450207). Its correct Golgi localization is required for its transforming activity, which engages PI3K/Akt and TGFβ signaling (PMID:22510613). In the liver, hepatocyte FNDC3B protects against alcohol-induced steatosis and ferroptosis by activating AMPK and maintaining transferrin expression to prevent iron overload (PMID:36336231). In the developing cerebellum, Purkinje-cell FNDC3B facilitates climbing fiber synapse elimination (PMID:41574767). FNDC3B expression is tightly controlled, being activated by E2F1 and repressed by numerous microRNAs and by circFNDC3B-associated machinery (PMID:36336231, PMID:38403291, PMID:38129874).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2004 Medium

    Established FNDC3B (FAD104) as an early, functionally required driver of adipocyte differentiation, the first assignment of a cellular role to the gene.

    Evidence RNAi knockdown and adipogenesis assays in 3T3-L1 cells

    PMID:15527760

    Open questions at the time
    • No molecular partner or signaling mechanism identified
    • Restricted to a single cell-line model of adipogenesis
  2. 2008 High

    In vivo knockout revealed FNDC3B is essential for postnatal survival and showed it governs cytoskeletal organization, adhesion, spreading, migration, and proliferation in primary cells, broadening its role beyond adipogenesis.

    Evidence Gene targeting in mice, MEF adhesion/wound-healing/proliferation assays

    PMID:19138685

    Open questions at the time
    • Molecular cause of neonatal lethality not yet defined
    • No mechanistic link between FNDC3B and stress fiber formation
  3. 2010 Medium

    Defined FNDC3B as a negative regulator of osteoblast differentiation, positioning it as a switch in the adipocyte-versus-osteoblast mesenchymal fate decision.

    Evidence Osteoblast differentiation assays and Runx2 western blot in knockout MEFs

    PMID:20493170

    Open questions at the time
    • Mechanism by which FNDC3B suppresses osteogenesis not yet identified
    • Relationship to BMP-2 signaling not resolved at this stage
  4. 2011 High

    Pinpointed the cause of neonatal lethality to lung dysplasia, identifying FNDC3B as essential for alveolar type II cell maturation and surfactant production.

    Evidence Knockout mouse phenotyping, immunohistochemistry, surfactant protein assays

    PMID:21704616

    Open questions at the time
    • Molecular pathway linking FNDC3B to ATII maturation not defined
    • No partner protein identified in lung context
  5. 2013 High

    Provided the first direct molecular mechanism, showing FNDC3B binds Smad1/5/8 via its N-terminal proline-rich motif to suppress BMP/Smad signaling, explaining the osteogenesis phenotype and a craniosynostosis-like skeletal defect.

    Evidence Co-IP, N-terminal deletion mutagenesis, in vitro phosphorylation, calvarial differentiation and knockout phenotyping

    PMID:24052261

    Open questions at the time
    • Structural basis of the Smad interaction not determined
    • How an ER/Golgi-anchored protein contacts cytoplasmic Smads not resolved
  6. 2015 Medium

    Extended FNDC3B's interaction repertoire to STAT3, demonstrating it suppresses STAT3 phosphorylation and melanoma invasion/metastasis, establishing a tumor-suppressive context.

    Evidence Co-IP, knockdown/overexpression, transwell invasion, in vivo lung colonization

    PMID:25671570

    Open questions at the time
    • Direct versus indirect nature of STAT3 dephosphorylation unclear
    • No reciprocal validation of the interaction
  7. 2016 Medium

    Mapped the STAT3 interaction to the FNDC3B N-terminal region (proline-rich plus transmembrane domain) and the STAT3 C-terminus, defining the structural determinants of suppression.

    Evidence Deletion mutant Co-IP and colony formation assays

    PMID:26948083

    Open questions at the time
    • No high-resolution interface defined
    • Generality of the N-terminal interaction module across partners not tested
  8. 2016 Medium

    Revealed a pro-migratory, oncogenic role in hepatocellular carcinoma through cooperation with ANXA2, contrasting with the STAT3-suppressive context and establishing FNDC3B as context-dependent.

    Evidence LC-MS/MS, mutagenesis, shRNA knockdown, migration/invasion and in vivo metastasis assays

    PMID:27385217

    Open questions at the time
    • Mechanism by which ANXA2 cooperation drives migration not detailed
    • Single-lab interaction without independent confirmation
  9. 2017 Medium

    Reconciled the dual role in EMT by showing FNDC3B differentially modulates TGFβ/Smad arms—suppressing Smad2/3 and promoting Smad1/5/8 phosphorylation—to inhibit TGFβ-induced EMT in cervical cancer.

    Evidence Overexpression/knockdown in HeLa cells with phospho-Smad and EMT marker readouts

    PMID:29180690

    Open questions at the time
    • Direct substrate-level mechanism for opposing Smad regulation unknown
    • Reconciliation with oncogenic contexts not addressed
  10. 2020 Medium

    Identified two additional oncogenic effector axes: MYH9 stabilization driving Wnt/β-catenin activation in nasopharyngeal carcinoma and PI3K/mTOR-driven proliferation in colorectal cancer.

    Evidence Co-IP, protein stability and Wnt reporter assays; proliferation/invasion assays with PI3K/mTOR western blots; in vivo tumor models

    PMID:32232887 PMID:32431508

    Open questions at the time
    • Whether MYH9 and ANXA2 use the same FNDC3B interface unknown
    • Single-lab findings per cancer type
  11. 2022 High

    Defined a protective metabolic function in the liver, with hepatocyte FNDC3B activating AMPK to limit steatosis and to maintain transferrin expression, thereby preventing ethanol-induced lipid peroxidation, iron overload, and ferroptosis.

    Evidence Hepatocyte-specific conditional knockout, AMPK activity assays, RNA-seq, ferrostatin-1 rescue

    PMID:36336231

    Open questions at the time
    • How FNDC3B activates AMPK mechanistically unknown
    • Direct molecular partners in the liver not identified
  12. 2024 Medium

    Added a transcriptional input by showing E2F1 directly activates FNDC3B in hepatocellular carcinoma to promote migration, complementing the extensive microRNA control of the gene.

    Evidence TF knockdown screening, ChIP-ddPCR, migration assays

    PMID:38403291

    Open questions at the time
    • Other transcriptional regulators not surveyed
    • Context-specificity of E2F1 control across tissues untested
  13. 2025 Medium

    Identified FAM83H as a partner stabilized by FNDC3B via the N-terminal proline-rich/transmembrane region, defining a FNDC3B/FAM83H/Snail/EMT axis driving gastric cancer metastasis.

    Evidence LC-MS/MS, Co-IP, domain mutants, ubiquitin-proteasome degradation assays, rescue, xenografts

    PMID:40450207

    Open questions at the time
    • Mechanism by which FNDC3B blocks FAM83H ubiquitination unknown
    • Single-lab interaction
  14. 2026 High

    Uncovered a neuronal role, with Purkinje-cell FNDC3B facilitating climbing fiber synapse elimination during cerebellar development, broadening its function into the nervous system.

    Evidence PC-specific conditional knockout, electrophysiology, CF morphology across postnatal timepoints with synaptic-input specificity controls

    PMID:41574767

    Open questions at the time
    • Molecular effectors mediating synapse elimination not identified
    • Whether known FNDC3B partners operate in neurons unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how a single ER/Golgi-anchored transmembrane protein mechanistically switches between tumor-suppressive (STAT3, BMP/Smad) and oncogenic (ANXA2, MYH9, FAM83H, PI3K/mTOR) outputs, and what unifies its developmental, metabolic, and neuronal roles.
  • No structural model of the N-terminal interaction module
  • No unified explanation for context-dependent partner selection
  • Topology question of how a membrane-anchored protein engages diverse cytoplasmic partners

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 3 GO:0060089 molecular transducer activity 2 GO:0140313 molecular sequestering activity 2
Localization
GO:0005783 endoplasmic reticulum 1 GO:0005794 Golgi apparatus 1 GO:0005886 plasma membrane 1
Pathway
R-HSA-1643685 Disease 4 R-HSA-1266738 Developmental Biology 3 R-HSA-162582 Signal Transduction 3 R-HSA-1430728 Metabolism 1

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 FNDC3B oncoprotein localizes to the Golgi network, and correct Golgi localization is essential for its transforming function. Overexpression induces EMT and activates PI3K/Akt, Rb1, and TGFβ signaling pathways. For TGFβ signaling, FNDC3B induces expression of all three TGFβ ligands and promotes TGFBR1 cell-surface localization. Cellular localization assays, RNAi knockdown, overexpression in mammary/kidney epithelial cells and hepatocytes, cancer pathway activation assays Cell cycle (Georgetown, Tex.) Medium 22510613
2004 Fad104 (FNDC3B) expression is rapidly induced in early adipogenesis and functions as a positive regulator of adipocyte differentiation; knockdown by RNAi represses adipogenesis in 3T3-L1 cells. RNAi knockdown, adipogenesis assays in 3T3-L1 cells FEBS letters Medium 15527760
2008 Disruption of fad104 (FNDC3B) in mice causes rapid postnatal death, and fad104-deficient MEFs show reduced stress fiber formation, delayed cell adhesion, spreading, and migration, as well as inhibited adipocyte differentiation and cell proliferation. Gene targeting (knockout mice), mouse embryonic fibroblast analysis, cell adhesion assays, wound healing assays Experimental cell research High 19138685
2010 Fad104 (FNDC3B) negatively regulates osteoblast differentiation: its expression decreases during osteogenesis, and fad104 deletion in MEFs facilitates osteoblast differentiation and elevates Runx2 levels. fad104 also suppresses BMP-2-mediated adipocyte differentiation. Gene knockout MEFs, osteoblast differentiation assays, western blot for Runx2 Biochemical and biophysical research communications Medium 20493170
2011 Fad104 (FNDC3B) is essential for lung maturation: fad104-deficient mice die due to lung dysplasia (atelectasis), FAD104 is strongly expressed in ATII cells in the developing lung, and its loss impairs ATII cell maturation and surfactant-associated protein expression. Knockout mouse phenotypic analysis, immunohistochemistry, surfactant protein expression assays Experimental cell research High 21704616
2013 FAD104 (FNDC3B) interacts with Smad1/5/8 via its N-terminal proline-rich motif and down-regulates Smad1/5/8 phosphorylation, acting as a negative regulator of BMP/Smad signaling in calvarial cells. fad104 disruption causes craniosynostosis-like premature calvarial ossification. Co-immunoprecipitation, mutagenesis (N-terminal deletion mutants), in vitro phosphorylation assays, calvarial cell differentiation assays, knockout mouse phenotyping The Journal of biological chemistry High 24052261
2015 Fad104 (FNDC3B) suppresses invasion and metastasis of melanoma cells by interacting with STAT3 and downregulating STAT3 phosphorylation. Reduction of fad104 enhanced migration/invasion; overexpression inhibited lung colonization. Co-immunoprecipitation, overexpression/knockdown, transwell invasion assays, in vivo lung colonization assay, phosphorylation assays PloS one Medium 25671570
2016 FAD104 (FNDC3B) N-terminal region (containing proline-rich motif and transmembrane domain) is required for interaction with the C-terminal region of STAT3 and suppression of STAT3 activity and anchorage-independent growth in melanoma cells. Deletion mutant analysis, co-immunoprecipitation, colony formation assays Biological & pharmaceutical bulletin Medium 26948083
2016 FNDC3B promotes cell migration in hepatocellular carcinoma by cooperating with annexin A2 (ANXA2); mutagenesis and LC-MS/MS analyses identified this interaction, and overexpression enhanced migration/invasion while shRNA knockdown reduced metastatic nodule formation. LC-MS/MS, mutagenesis, shRNA knockdown, cell migration/invasion assays, in vivo metastasis models Oncotarget Medium 27385217
2017 FAD104 (FNDC3B) functions as a suppressor of TGF-β-mediated EMT in cervical cancer cells: FAD104 overexpression suppresses TGF-β-induced EMT, negatively regulates phosphorylation of Smad2 and Smad3, and positively regulates phosphorylation of Smad1/5/8. Overexpression and knockdown in HeLa cells, TGF-β treatment, phosphorylation assays (western blot), EMT marker analysis Scientific reports Medium 29180690
2013 FNDC3B protein (not mRNA) is repressed by miR-143 in prostate cancer cells; luciferase reporter assays confirmed FNDC3B as a direct miR-143 target that regulates cell motility. Luciferase reporter assay, western blot, transwell/wound healing assays, in vivo bioluminescence imaging BMC cancer Medium 23383988
2016 miR-215-5p directly targets FNDC3B (and CTNNBIP1) to impair adipocyte differentiation in 3T3-L1 cells, placing FNDC3B downstream of miR-215-5p in the regulation of early adipogenesis. Luciferase reporter assay, overexpression/knockdown, adipogenesis assays in 3T3-L1 cells The international journal of biochemistry & cell biology Medium 27521659
2020 FNDC3B binds to and stabilizes myosin heavy chain 9 (MYH9) to activate the Wnt/β-catenin signaling pathway in nasopharyngeal carcinoma; 3'-UTR shortening via alternative polyadenylation escapes miRNA-mediated repression, causing FNDC3B overexpression. Co-immunoprecipitation, knockdown/overexpression, protein stability assays, Wnt/β-catenin reporter assays, in vitro and in vivo tumor models Cancer science Medium 32232887
2022 Hepatocyte-specific FNDC3B deletion aggravates alcohol-induced liver steatosis via AMPK inhibition. FNDC3B deletion also exacerbates ethanol-mediated lipid peroxidation and ferroptosis through AMPK inactivation, which downregulates transferrin expression and causes iron overload. FNDC3B expression is negatively regulated by miR-192-5p. Hepatocyte-specific conditional knockout mice, AMPK activity assays, RNA sequencing, ferroptosis inhibitor rescue (ferrostatin-1), primary hepatocyte studies Free radical biology & medicine High 36336231
2020 FNDC3B promotes proliferation and invasion of colorectal cancer cells via PI3K/mTOR signaling; miR-125a-5p and miR-217 directly bind FNDC3B 3'-UTR (binding motifs CUCAGGG and AUGCAGU respectively) and suppress its expression. Luciferase reporter assay, CCK-8/MTT proliferation assays, transwell invasion, western blot for PI3K/mTOR pathway components OncoTargets and therapy Medium 32431508
2024 E2F1 transcription factor directly activates FNDC3B transcription in hepatocellular carcinoma, identified via TF knockdown screening and ChIP coupled with Droplet Digital PCR; E2F1 overexpression or knockdown significantly impacts FNDC3B expression and downstream cell migration. ChIP-seq database analysis, TF knockdown screening, ChIP-ddPCR, overexpression/knockdown assays FEBS open bio Medium 38403291
2025 FNDC3B interacts with FAM83H via its proline-rich N-terminus and transmembrane domain, preventing FAM83H ubiquitin-proteasomal degradation, thereby promoting gastric cancer metastasis through the FNDC3B/FAM83H/Snail/EMT axis. LC-MS/MS, co-immunoprecipitation, truncated domain mutants, immunofluorescence, ubiquitin-proteasome degradation assays, rescue experiments, in vivo xenograft models Cellular & molecular biology letters Medium 40450207
2017 miR-34a suppresses ESCC cell migration and invasion by directly targeting FNDC3B (via its 3'-UTR) as well as MMP-2 and MMP-9; luciferase reporter assays and western blot confirmed FNDC3B as a direct miR-34a target. Luciferase reporter assay, western blot, wound healing and transwell assays International journal of oncology Medium 28534990
2015 FNDC3B promotes EMT in tongue squamous cell carcinoma under hypoxic conditions: CoCl2 (hypoxia mimetic) upregulates FNDC3B mRNA and protein via HIF-1α, and FNDC3B knockdown suppresses migratory and invasive abilities. HIF-1α regulation study, shRNA knockdown, transwell migration/invasion assays, western blot Oncology reports Medium 29393475
2026 FNDC3B (as an ER-anchored protein expressed in Purkinje cells) facilitates climbing fiber synapse elimination in the developing mouse cerebellum from postnatal day 9–10; PC-specific conditional knockout impairs CF synapse elimination and reduces CF extension along PC dendrites at P21, with recovery by P40. Parallel fiber and inhibitory synaptic inputs are not affected. PC-specific RNAi knockdown screening, conditional knockout mice (FNDC3B-cKO), electrophysiology, morphological analysis of CF innervation The European journal of neuroscience High 41574767
2023 RNA binding protein RBM47 binds flanking introns of FNDC3B pre-mRNA to facilitate back-splicing and generation of circFNDC3B, leading to reduction of FNDC3B mRNA levels. CircFNDC3B also inhibits FNDC3B mRNA stability by competitively binding to IGF2BP1, creating an imbalance between circFNDC3B (tumor suppressor) and FNDC3B mRNA (oncogene) in osteosarcoma. RIP assay, RNA stability analysis, RNA-FISH, immunofluorescence, qRT-PCR, functional assays Cancer cell international Medium 38129874

Source papers

Stage 0 corpus · 53 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2019 FNDC3B circular RNA promotes the migration and invasion of gastric cancer cells via the regulation of E-cadherin and CD44 expression. Journal of cellular physiology 100 30963578
2013 Up-regulated microRNA-143 in cancer stem cells differentiation promotes prostate cancer cells metastasis by modulating FNDC3B expression. BMC cancer 86 23383988
2012 Activation of multiple cancer pathways and tumor maintenance function of the 3q amplified oncogene FNDC3B. Cell cycle (Georgetown, Tex.) 69 22510613
2004 The novel gene fad104, containing a fibronectin type III domain, has a significant role in adipogenesis. FEBS letters 60 15527760
2021 Circular RNA FNDC3B Protects Oral Squamous Cell Carcinoma Cells From Ferroptosis and Contributes to the Malignant Progression by Regulating miR-520d-5p/SLC7A11 Axis. Frontiers in oncology 53 34434890
2022 FNDC3B protects steatosis and ferroptosis via the AMPK pathway in alcoholic fatty liver disease. Free radical biology & medicine 49 36336231
2017 Tumor suppressor microRNA-34a inhibits cell migration and invasion by targeting MMP-2/MMP-9/FNDC3B in esophageal squamous cell carcinoma. International journal of oncology 49 28534990
2017 Potential mechanisms of microRNA-129-5p in inhibiting cell processes including viability, proliferation, migration and invasiveness of glioblastoma cells U87 through targeting FNDC3B. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 45 28068630
2016 FNDC3B promotes cell migration and tumor metastasis in hepatocellular carcinoma. Oncotarget 41 27385217
2008 Disruption of the novel gene fad104 causes rapid postnatal death and attenuation of cell proliferation, adhesion, spreading and migration. Experimental cell research 39 19138685
2020 FNDC3B 3'-UTR shortening escapes from microRNA-mediated gene repression and promotes nasopharyngeal carcinoma progression. Cancer science 32 32232887
2010 Fad104, a positive regulator of adipogenesis, negatively regulates osteoblast differentiation. Biochemical and biophysical research communications 29 20493170
2016 MicroRNA-215 impairs adipocyte differentiation and co-represses FNDC3B and CTNNBIP1. The international journal of biochemistry & cell biology 25 27521659
2022 Exosomal circRNA FNDC3B promotes the progression of esophageal squamous cell carcinoma by sponging miR-490-5p and regulating thioredoxin reductase 1 expression. Bioengineered 24 35703190
2020 FNDC3B, Targeted by miR-125a-5p and miR-217, Promotes the Proliferation and Invasion of Colorectal Cancer Cells via PI3K/mTOR Signaling. OncoTargets and therapy 24 32431508
2018 FNDC3B promotes epithelial-mesenchymal transition in tongue squamous cell carcinoma cells in a hypoxic microenvironment. Oncology reports 24 29393475
2015 Fad104, a positive regulator of adipocyte differentiation, suppresses invasion and metastasis of melanoma cells by inhibition of STAT3 activity. PloS one 23 25671570
2017 FAD104, a regulator of adipogenesis, is a novel suppressor of TGF-β-mediated EMT in cervical cancer cells. Scientific reports 22 29180690
2024 A novel protein FNDC3B-267aa encoded by circ0003692 inhibits gastric cancer metastasis via promoting proteasomal degradation of c-Myc. Journal of translational medicine 19 38802851
2013 FAD104, a regulatory factor of adipogenesis, acts as a novel regulator of calvarial bone formation. The Journal of biological chemistry 19 24052261
2021 Curcumin suppresses renal carcinoma tumorigenesis by regulating circ-FNDC3B/miR-138-5p/IGF2 axis. Anti-cancer drugs 18 34001703
1998 Sonodynamically-induced cell damage with fluorinated anthracycline derivative, FAD104. Cancer letters 18 9566717
2021 Identification of Circ-FNDC3B, an Overexpressed circRNA in Abdominal Aortic Aneurysm, as a Regulator of Vascular Smooth Muscle Cells. International heart journal 16 34789642
2021 MicroRNA-363-3p promote the development of acute myeloid leukemia with RUNX1 mutation by targeting SPRYD4 and FNDC3B. Medicine 14 33950983
2020 Novel lncRNA XLOC_032768 protects against renal tubular epithelial cells apoptosis in renal ischemia-reperfusion injury by regulating FNDC3B/TGF-β1. Renal failure 14 32972270
2011 Indispensable role of factor for adipocyte differentiation 104 (fad104) in lung maturation. Experimental cell research 12 21704616
2021 CircSOS2 promotes cervical squamous cell carcinoma by regulation of proliferation, cell cycle, apoptosis, migration, invasion, and glycolysis by targeting miR-543/FNDC3B axis. Archives of biochemistry and biophysics 11 34023283
2020 MiR-1225-5p acts as tumor suppressor in glioblastoma via targeting FNDC3B. Open medicine (Warsaw, Poland) 11 33336045
2021 lncRNA LINC00355 Acts as a Novel Biomarker and Promotes Glioma Biological Activities via the Regulation of miR-1225/FNDC3B. Disease markers 10 34603558
2022 CircRNA hsa_circ_0001627 aggravates cervical cancer progression through upregulation of FNDC3B and activating PI3K/mTOR signaling pathway. Journal of cell communication and signaling 9 36357650
2023 A RBM47 and IGF2BP1 mediated circular FNDC3B-FNDC3B mRNA imbalance is involved in the malignant processes of osteosarcoma. Cancer cell international 8 38129874
2022 Evaluation of ABCA1 and FNDC3B Gene Polymorphisms Associated With Pseudoexfoliation Glaucoma and Primary Angle-Closure Glaucoma in a Saudi Cohort. Frontiers in genetics 8 35719397
2021 FNDC3B and BPGM Are Involved in Human Papillomavirus-Mediated Carcinogenesis of Cervical Cancer. Frontiers in oncology 8 34976823
1988 Biological properties of ME2303 (FAD-104), a new anthracycline. Drugs under experimental and clinical research 8 3240704
2023 Circ_0000285 regulates nasopharyngeal carcinoma progression through miR-1278/FNDC3B axis. Human & experimental toxicology 7 36738165
2024 E2F1 promotes cell migration in hepatocellular carcinoma via FNDC3B. FEBS open bio 6 38403291
2016 Two cases with de novo 3q26.31 microdeletion suggest a role for FNDC3B in human craniofacial development. American journal of medical genetics. Part A 6 27541078
2016 FAD104, a Regulator of Adipogenesis and Osteogenesis, Interacts with the C-Terminal Region of STAT3 and Represses Malignant Transformation of Melanoma Cells. Biological & pharmaceutical bulletin 5 26948083
1990 Biological activities of new anthracyclines containing fluorine, FAD104 and its metabolites. The Journal of antibiotics 5 1694165
2023 Circ-FNDC3B Functions as an Oncogenic Factor in Esophageal Squamous Cell Carcinoma via Upregulating MYO5A by Absorbing miR-136-5p and miR-370-3p. Biochemical genetics 4 36884165
2023 Clinical and genomic characterization of an ATRA-insensitive acute promyelocytic leukemia variant with a FNDC3B::RARB fusion. Genes, chromosomes & cancer 4 37283355
2021 Expression of NR5A2, NUP153, HNF4A, USP15 and FNDC3B is consistent with their use as novel biomarkers for bovine mammary stem/progenitor cells. Journal of molecular histology 4 33400051
2025 Blocking circular RNA FNDC3B induces fibroblast-like synoviocytes dysfunction to ameliorate rheumatoid arthritis through regulating the miR-125a-5p-Hexokinase2 axis. Cytotechnology 2 40160441
2025 FNDC3B promotes gastric cancer metastasis via interacting with FAM83H and preventing its proteasomal degradation. Cellular & molecular biology letters 2 40450207
2024 Circ_FNDC3B Promotes Cell Proliferation and Metastasis in Esophageal Squamous Cell Carcinoma via Regulating MAPK1 by Binding to miR-136-5p. Biochemical genetics 2 38228844
2026 Multifaceted roles of fibronectin type III domain containing 3B (FNDC3B) in cell biology and signaling. Frontiers in molecular biosciences 1 41704736
2022 Long Non-Coding RNA DUXAP8 Acts as an Oncogene in Sinonasal Squamous Cell Carcinoma Through miR-584-5p/FNDC3B Pathway. American journal of rhinology & allergy 1 35695194
2021 [Corrigendum] FNDC3B promotes epithelial‑mesenchymal transition in tongue squamous cell carcinoma cells in a hypoxic microenvironment. Oncology reports 1 33907845
2026 The ER/Golgi Protein FNDC3B Facilitates Climbing Fibre to Purkinje Cell Synapse Elimination in the Developing Mouse Cerebellum. The European journal of neuroscience 0 41574767
2026 Let-7a and miR-34a Interplay Potent Suppressive Roles in Hepatocellular Carcinoma via Co-Targeting FNDC3B, IGF2 and SOX4. International journal of molecular sciences 0 41751849
2026 SF3B4-QKI splicing complex generates circ-FNDC3B and mediates breast cancer inhibition. Molecular cancer research : MCR 0 41837881
2026 CDNFE suggests FNDC3B and NECTIN4 as drivers of precancer progression via PI3K/AKT EMT. NPJ precision oncology 0 42032137
2020 [Corrigendum] FNDC3B promotes epithelial-mesenchymal transition in tongue squamous cell carcinoma cells in a hypoxic microenvironment. Oncology reports 0 33106884

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