| 1998 |
PCDH9 is a member of the protocadherin subfamily of calcium-dependent cell-cell adhesion and recognition proteins. It is predominantly expressed in brain but also in a broader variety of tissues, with developmentally regulated expression patterns. |
Gene isolation, genomic organization analysis, expression profiling |
Genomics |
Medium |
9787079
|
| 2013 |
Restoration of PCDH9 expression in glioma cell lines (U87 and U251) reduced tumor cell viability, induced apoptosis, caused G0/G1 cell cycle arrest, and suppressed colony formation and invasion. Molecularly, PCDH9 restoration upregulated Bax protein and downregulated Bcl-2 and cyclin D1. |
Lentiviral PCDH9 re-expression in glioma cell lines, cell viability assays, apoptosis assays, cell cycle analysis, invasion assays, Western blot |
Journal of molecular neuroscience : MN |
Medium |
24214103
|
| 2015 |
Pcdh9 knockout mice exhibit specific long-term social and object recognition deficits, early touch-evoked biting, rotarod performance deficits, and sensory gating deficits. Structural changes were observed in deep layers of sensory cortices, where Pcdh9 is selectively expressed, implicating PCDH9 in sensory cortex development and long-term memory functions. |
Chromosome substitution strain QTL mapping, Pcdh9 knockout mouse generation, behavioral testing, gene expression analysis, brain morphology analysis |
Biological psychiatry |
High |
25802080
|
| 2017 |
miR-215-5p suppresses PCDH9 expression in glioma by targeting both the promoter and 3'UTR of PCDH9 simultaneously (dual inhibition), leading to increased glioma cell proliferation, clone formation, migration, and reduced apoptosis. |
Luciferase reporter assays (promoter and 3'UTR), qRT-PCR, Western blot, cell proliferation, migration, and apoptosis assays in glioma cell lines |
Oncotarget |
Medium |
28055966
|
| 2017 |
PCDH9 promoter methylation leads to transcriptional silencing in hepatocellular carcinoma (HCC), and treatment with DNA demethylation agent 5-azacytidine restores PCDH9 expression. Restored PCDH9 expression inhibits HCC cell proliferation and xenograft tumor formation by inducing G0/G1 cell cycle arrest. |
Quantitative methylation analysis, 5-azacytidine treatment, PCDH9 re-expression, cell proliferation assays, xenograft tumor formation, cell cycle analysis |
Molecular medicine reports |
Medium |
28791409
|
| 2019 |
miR-200a-3p directly binds the 3'-UTR of PCDH9 mRNA and decreases PCDH9 expression in ovarian cancer cells, thereby promoting ovarian cancer cell proliferation, colony formation, and invasion. Restoring PCDH9 expression inhibits the pro-proliferative effect of miR-200a-3p. |
Luciferase reporter assay (3'UTR), qRT-PCR, Western blot, cell proliferation, colony formation, invasion assays, rescue experiments |
OncoTargets and therapy |
Medium |
31632082
|
| 2022 |
COP1 (RFWD2), a RING-finger E3 ubiquitin ligase, physically interacts with PCDH9 and promotes its Lys48-linked polyubiquitination and proteasomal degradation in glioma cells. COP1 protein levels are inversely correlated with PCDH9 protein levels in human glioma tissues. |
Yeast two-hybrid screen, co-immunoprecipitation, immunofluorescence co-localization, ubiquitination assays, proteasome inhibitor experiments, Western blot, human glioma tissue analysis |
Molecular neurobiology |
High |
35084653
|
| 2022 |
PCDH9 overexpression in melanoma inhibits cell proliferation and migration, downregulates RAC1, MMP2, and MMP9, and upregulates Pyk2 and Cyclin D1. The circ_0084043/miR-134-5p axis indirectly regulates PCDH9: circ_0084043 sponges miR-134-5p, thereby relieving miR-134-5p-mediated suppression of PCDH9. PCDH9 overexpression also inhibits melanoma tumor growth in vivo. |
Lentiviral overexpression/knockdown of PCDH9, proliferation/invasion/apoptosis assays, qRT-PCR, Western blot, in vivo xenograft, ceRNA luciferase reporter assays |
Frontiers in oncology |
Medium |
36387162
|
| 2024 |
PCDH9 is cleaved in gastric cancer cells, generating an intracellular domain (ICD) that translocates to the nucleus. In the nucleus, the PCDH9 ICD interacts with DNA methyltransferase 1 (DNMT1) and increases DNMT1 activity, which leads to increased DNA methylation at the CDH2 (N-cadherin) promoter, downregulating CDH2 expression and thereby dampening gastric cancer cell migration and in vivo metastasis. |
Co-immunoprecipitation, nuclear fractionation, DNMT1 activity assays, DNA methylation analysis (promoter bisulfite), cell migration assays, in vivo metastasis models, correlation with patient tissue data |
iScience |
High |
38357662
|
| 2024 |
PCDH9 primarily localizes at glutamatergic synapses in the mouse hippocampus CA1 region, with expression peaking in the first week after birth. Pcdh9 KO neurons exhibit oversized presynaptic terminals and postsynaptic densities, widespread upregulation of synaptic genes (by snRNA-seq), dysregulation of the SHANK2/CORTACTIN pathway, increased miniature excitatory postsynaptic currents (mEPSC), and reduced network activity in CA1. |
Pcdh9 KO mice, electron microscopy (ultrastructural), single-nucleus RNA-seq, electrophysiology (mEPSC recordings), biochemical fractionation/localization, network activity recordings |
The Journal of neuroscience |
High |
39557582
|
| 2026 |
Neuronal activity triggers Matrix Metalloprotease (MMP)-dependent cleavage of PCDH9, generating a C-terminal fragment (CTF) that translocates to the nucleus. Overexpression of the PCDH9 CTF promotes dendritic growth, increases spine density, and strengthens excitatory synaptic transmission, identifying PCDH9 CTF as an activity-dependent signaling molecule linking synaptic activity to structural and functional remodeling. |
Biochemical fractionation, immunohistochemistry, MMP inhibitor treatment, neuronal cultures, CTF overexpression, dendritic morphology analysis, spine density quantification, electrophysiology |
Frontiers in cellular neuroscience |
Medium |
41685090
|
| 2026 |
RNF145, an E3 ubiquitin ligase, physically interacts with PCDH9 and promotes its ubiquitination and subsequent proteasomal degradation, thereby facilitating hepatocellular carcinoma cell migration and invasion. Knockdown of RNF145 abolishes migratory and invasive capacities of HCC cells. |
Co-immunoprecipitation, Western blot, ubiquitination assays, transwell migration/invasion assays, wound-healing assay, RNF145 knockdown |
Oncology research |
Medium |
41613811
|