| 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
|