| 2004 |
CDH11 promoter drives high-level transcriptional activation of USP6 oncogene in primary aneurysmal bone cysts via chromosomal translocation, creating a CDH11-USP6 fusion gene; rearrangements were restricted to spindle cells and absent in multinucleated giant cells, inflammatory cells, endothelial cells, and osteoblasts. |
FISH/cytogenetics, molecular rearrangement analysis on primary tumor tissue |
The American journal of pathology |
Medium |
15509545
|
| 2010 |
Cdh11 loss-of-function in murine retinoblastoma promotes tumor cell survival by reducing cell death (5- to 10-fold decrease in apoptotic markers including activated caspase-3) without affecting proliferation; Cdh11 knockdown in vitro increases β-catenin expression, placing Cdh11 as a pro-apoptotic tumor suppressor upstream of β-catenin. |
Cdh11 knockout mouse crossed with TAg-RB tumor model; in vitro siRNA knockdown with caspase-3 and β-catenin immunostaining; in vivo tumor volume and cell death quantification |
PLoS genetics |
High |
20421947
|
| 2015 |
miR-27b directly targets the CDH11 3'UTR to suppress CDH11 expression, and CDH11 mediates epithelial-mesenchymal transition (EMT) by regulating E-cadherin, vimentin, and N-cadherin expression in cervical cancer cells. |
miR-27b overexpression/inhibition, CDH11 cDNA rescue transfection, siRNA knockdown, proliferation and invasion assays, EMT marker immunoblotting |
Oncology reports |
Medium |
26706910
|
| 2018 |
FOXF1 transcription factor directly binds Cdh2 and Cdh11 promoters to differentially regulate their transcription; FOXF1 deletion promotes a switch from N-cadherin (CDH2) to Cadherin-11 (CDH11) in lung myofibroblasts, which is a critical step driving pro-fibrotic myofibroblast invasion and collagen secretion. Re-expression of CDH2 or inhibition of CDH11 in FOXF1-deficient cells reduces myofibroblast invasion. |
Fibroblast-specific FOXF1 knockout mice, chromatin immunoprecipitation (ChIP) on Cdh2/Cdh11 promoters, in vitro invasion assays with CDH11 inhibition and CDH2 re-expression rescue |
Cell reports |
High |
29642003
|
| 2018 |
CDH11 promotes liver fibrosis by activating hepatic stellate cells (HSCs); CDH11 mediates TGFβ-induced HSC activation, and CDH11-deficient mouse HSCs show decreased activation in vitro and reduced fibrogenesis in vivo following CCl4-induced chronic liver injury. |
CDH11-deficient mouse model, CCl4-induced fibrosis in vivo, in vitro HSC activation assays, TGFβ stimulation experiments |
Biochemical and biophysical research communications |
Medium |
30509494
|
| 2019 |
EPHB6 mutation induces paclitaxel resistance via interaction with EPHA2, which promotes JNK-mediated CDH11 expression; elevated CDH11 then mediates cell adhesion-mediated drug resistance (CAM-DR) through RhoA/FAK activation. Targeted inhibition of CDH11 reversed acquired paclitaxel resistance. |
EPHB6 mutation cell line models, kinase inhibitor experiments, CDH11 siRNA knockdown, RhoA/FAK signaling readouts, drug resistance assays |
Experimental & molecular medicine |
Medium |
31160603
|
| 2019 |
In metastatic breast cancer cells co-cultured with CDH11-rich cancer-associated fibroblasts, anti-CDH11 antibody suppresses CDH11, β-catenin, fibronectin, and vimentin expression, abrogating cancer stem cell-like traits and metastasis; ectopic miR-335 expression suppresses CDH11 and downstream β-catenin/vimentin, while CDH11 inhibition upregulates miR-335. |
Anti-CDH11 monoclonal antibody treatment, miR-335 mimic/inhibitor transfection, co-culture with CAFs, in vivo xenograft tumor models, protein expression analysis |
BMC cancer |
Medium |
31248373
|
| 2019 |
C12orf59 upregulates CDH11 expression via NF-κB signaling; in turn, CDH11 promotes NF-κB binding to the C12orf59 promoter, forming a positive feedback loop that sustains gastric cancer cell metastatic ability. |
Gain- and loss-of-function studies in vitro and in vivo, NF-κB pathway inhibition, promoter binding assays, invasion/metastasis assays |
Journal of experimental & clinical cancer research : CR |
Medium |
30987656
|
| 2021 |
Pathogenic CDH11 heterozygous missense variants clustered around EC2-EC3 and EC3-EC4 linker regions (predicted to affect Ca2+ binding required for cadherin stability) significantly reduced cell-substrate trans adhesion activity; one EC3-EC4 linker variant caused changes in cell morphology, focal adhesion, and migration, suggesting a dominant negative effect. CDH11 protein is strongly expressed in human facial mesenchyme. |
Cell-substrate trans adhesion functional assays, cell morphology and focal adhesion imaging, migration assays, immunohistochemistry of human facial mesenchyme, exome sequencing validation |
Human genetics |
Medium |
33811546
|
| 2021 |
Exosomal miR-127-3p from bone marrow-derived mesenchymal stem cells inhibits CDH11 in chondrocytes, blocking Wnt/β-catenin pathway activation; overexpression of CDH11 reverses the protective exosome effects by reactivating Wnt/β-catenin signaling in IL-1β-injured chondrocytes. |
Exosome isolation and transfer, miR-127-3p inhibition, CDH11 overexpression rescue, Wnt/β-catenin pathway readouts, IL-1β chondrocyte injury model |
Journal of pain research |
Medium |
33574696
|
| 2021 |
CDH11 overexpression in tongue squamous cell carcinoma cells increases adhesion to human oral epithelial cells and decreases their ability to undergo transcellular migration through epithelial cells, acting as a tumor suppressor for invasion without affecting proliferation, apoptosis, stemness, or direct migration. |
CDH11 overexpression, adhesion assays with oral epithelial cells, transcellular migration assays, proliferation and apoptosis assays |
OncoTargets and therapy |
Medium |
34295163
|
| 2021 |
Cdh11-null mice (but not Cdh9-null mice) display multiple autism-like behavioral alterations, supporting a functional role for CDH11 in the neural circuits underlying autism spectrum disorder behaviors. |
Cdh11 knockout mouse behavioral studies (autism-relevant behavioral battery), comparison with Cdh9 knockout mice |
Neuroscience bulletin |
Medium |
34523068
|
| 2022 |
Extracellular vesicles (EVs) from RUNX2-high breast cancer cells deliver CDH11 protein to osteoblasts, mediating specific EV recognition and inducing an osteogenic premetastatic niche; CDH11 in EVs works together with ITGA5 to facilitate subsequent bone colonization of breast cancer cells. |
In vitro and in vivo EV transfer assays, CDH11/ITGA5 protein identification in EVs by proteomics, osteoblast education experiments, breast cancer bone metastasis mouse models |
Cancer research |
Medium |
35149589
|
| 2023 |
miR-101-3p directly targets CDH11 (and SOX9); inhibition of miR-101-3p restores CDH11 and SOX9 expression and prevents osteogenic differentiation/calcification of human aortic valve interstitial cells under calcific conditions. |
miR-101-3p mimic/inhibitor in primary HAVICs, CDH11/SOX9 expression readouts, calcification assays under osteogenic conditioned medium |
Molecular medicine (Cambridge, Mass.) |
Medium |
36809926
|
| 2023 |
FOXF1 overexpression inhibits TGF-β1-induced bronchial epithelial cell injury, fibrosis, and EMT by suppressing CDH11 expression and CDH11-mediated Wnt/β-catenin pathway activation; CDH11 overexpression reverses these protective FOXF1 effects. |
FOXF1 and CDH11 overexpression in TGF-β1-treated BEAS-2B cells, Wnt/β-catenin pathway protein readouts, fibrosis/EMT marker analysis, proliferation and apoptosis assays |
Experimental and therapeutic medicine |
Medium |
36798677
|
| 2024 |
YTHDF1 (an m6A reader) promotes CDH11 translation by reading m6A-enriched sites on CDH11 transcripts, as demonstrated by RIP-seq and MeRIP-seq; increased CDH11 expression downstream of YTHDF1 promotes breast cancer osteoblast adhesion and facilitates bone metastasis. |
RNA-seq, MeRIP-seq, RIP-seq, molecular biology (YTHDF1 knockdown/overexpression), AAV-mediated shYTHDF1 delivery in intratibial injection models |
Cancer letters |
Medium |
38871245
|
| 2024 |
CDH11 inhibits branched-chain ketoacid dehydrogenase to activate the mTOR pathway by interfering with branched-chain amino acid (BCAA) metabolism; CDH11 inhibitors (celecoxib and derivatives) regulate BCAA metabolism, increase ROS production, and activate the cGAS-STING pathway, suppressing lung metastasis in vivo. |
Single-cell RNA sequencing, spatial transcriptomics, CDH11 inhibitor treatment, BCAA metabolism assays, ROS measurement, cGAS-STING pathway readouts, NOD-SCID mouse lung metastasis models |
Advanced science (Weinheim, Baden-Wurttemberg, Germany) |
Medium |
39739317
|
| 2025 |
CDH11 knockdown in advanced bladder cancer cell lines suppresses mitochondrial metabolic activity (confirmed by Flux analyzer) and inhibits tumor growth in vivo, without affecting proliferation, invasion, or migration in vitro; a CDH11 inhibitor similarly decreases mitochondrial activity in vitro and suppresses tumor growth in vivo. |
shRNA-mediated CDH11 knockdown, RNA-seq, metabolic flux analysis, subcutaneous xenograft mouse model, CDH11 inhibitor treatment |
Cancer medicine |
Medium |
41263259
|
| 2025 |
CDH11 promotes airway neutrophilic inflammation in severe asthma via FGFR1 signaling; intratracheal instillation of recombinant CDH11 recruits neutrophils to the lungs, and this recruitment is blocked by FGFR1 inhibition. Pharmacological CDH11 antagonism (SD133) reduces airway neutrophil accumulation and IL-6/TNF-α production without affecting eosinophilic or type 2 inflammation. |
Murine severe asthma models (TDI and OVA/CFA), CDH11 antagonist SD133, recombinant CDH11 intratracheal instillation, FGFR1 inhibitor experiments, bronchoalveolar lavage cytology, cytokine measurement |
FASEB journal |
Medium |
41329017
|
| 2025 |
CDH11 knockdown in esophageal squamous cell carcinoma suppresses proliferation and invasion, while overexpression enhances them; CDH11 knockdown attenuates JAK-STAT3 and AKT signaling. Celecoxib and DMC directly bind CDH11 and inhibit ESCC growth in vitro and in vivo. |
CDH11 siRNA knockdown and overexpression, JAK-STAT3/AKT signaling readouts, direct drug-CDH11 binding assay, xenograft mouse model |
Pathology, research and practice |
Medium |
40460640
|
| 2025 |
USP14 deubiquitinase stabilizes CDH11 protein through deubiquitination; USP14 knockdown decreases CDH11 protein levels, and CDH11 overexpression rescues USP14 knockdown effects in IL-1β-stimulated chondrocytes, identifying USP14 as the deubiquitinating writer that prevents CDH11 proteasomal degradation. |
USP14 knockdown, CDH11 overexpression rescue, ubiquitination/deubiquitination assays, cell viability/apoptosis/ferroptosis readouts in IL-1β chondrocyte model |
Clinical rheumatology |
Medium |
41653235
|
| 2026 |
CDH11 promotes EMT and gastric cancer progression by upregulating TGF-β1 and activating TGF-β signaling; activated TGF-β signaling in turn enhances CDH11 transcription via binding of downstream transcription factor Snail2 to the CDH11 promoter, forming a positive feedback loop regulating invasion and metastasis. |
CDH11 gain/loss-of-function in GC cells, TGF-β1 expression and signaling readouts, Snail2 promoter binding assays, in vitro migration/invasion assays, lung metastasis in vivo model |
Translational oncology |
Medium |
42127732
|
| 2026 |
miR-205a directly binds the 3'UTR of CDH11 mRNA (confirmed by dual-luciferase assay) and inhibits chondrocyte differentiation by suppressing CDH11; CDH11 functions as a positive regulator of chondrocyte differentiation by promoting Wnt/β-catenin signaling. Silencing miR-205a or overexpressing CDH11 promotes chondrogenesis via Wnt/β-catenin and upregulates Runx2 and BMP2. |
Dual-luciferase reporter assay for miR-205a/CDH11 3'UTR binding, miR-205a overexpression/silencing, CDH11 overexpression, Wnt/β-catenin pathway agonist rescue, chondrogenic differentiation markers (Runx2, BMP2) in avian embryonic models |
Cell death discovery |
Medium |
42091868
|
| 2025 |
CDH11 knockout in lung fibroblasts suppresses fibroblast activation metrics (spreading and type I collagen expression), reduces Piezo1 expression, and decreases IL-6 secretion; blocking IL-6 signaling decreases CDH11 but not Piezo1 expression, establishing CDH11 as downstream of IL-6 and upstream of Piezo1/IL-6 in a feedforward fibroblast activation loop. |
CDH11 knockout fibroblasts in HA hydrogel platform, Piezo1 inhibition experiments, IL-6 signaling blockade, fibroblast-M2 macrophage co-culture, type I collagen expression and cell spreading readouts |
bioRxivpreprint |
Medium |
bio_10.1101_2025.09.16.674909
|
| 2017 |
Loss-of-function mutations in CDH11 (homozygous truncating/indel variants) cause Elsahy-Waters syndrome; patient fibroblasts show absent CDH11 protein expression, decreased cell proliferation rate, and delayed osteogenic differentiation potential compared to heterozygous parent and healthy donors. |
Exome sequencing and Sanger validation, immunostaining for CDH11 in patient-derived fibroblasts, cell proliferation assays, osteogenic differentiation assays |
American journal of medical genetics. Part A |
Medium |
28988429
|
| 2025 |
Transcription factors SP1 and GR bind to the CDH11 gene promoter core region (at -36/-27 bp and -20/-11 bp relative to TSS, respectively) to regulate CDH11 expression in bovine skeletal muscle, as identified by dual luciferase reporter assays with the core regulatory region mapped to -129/+55 bp. |
Dual luciferase reporter assays, promoter deletion constructs, transcription factor binding site analysis, tissue expression analysis |
Animals |
Low |
40362031
|