| 1998 |
Cap43/NDRG1 expression is specifically induced by Ni2+ compounds via elevation of free intracellular Ca2+; induction was attenuated by intracellular Ca2+ chelation and mimicked by calcium ionophores, establishing Ca2+ as the primary intracellular signal for nickel-mediated Cap43 induction. |
mRNA differential display, pharmacological manipulation (Ca2+ ionophores, BAPTA-AM chelator, okadaic acid), Northern blot in multiple human/rodent cell lines and rat organs |
Cancer research |
Medium |
9605764
|
| 1997 |
TDD5/NDRG1 mRNA expression is differentially repressed by testosterone and dihydrotestosterone (DHT) at the mRNA level in androgen-responsive cells, with testosterone showing preferential repression over DHT. |
mRNA differential display PCR (DDPCR), Northern blot, in vivo animal DHT administration studies |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
9144177
|
| 2004 |
NDRG1 is a p53-regulated gene induced by DNA damage in a p53-dependent manner; the NDRG1 promoter contains a p53 binding site conferring p53-dependent transcriptional activation. NDRG1 is necessary but not sufficient for p53-mediated caspase activation and apoptosis. |
Promoter-reporter assay, RNA interference (RNAi), inducible gene expression, caspase activation assays |
The Journal of biological chemistry |
High |
15377670
|
| 2004 |
Hypoxic induction of NDRG1 is predominantly dependent on the HIF-1 transcription factor, but HIF-1-independent pathways also contribute during chronic hypoxia. Nickel compounds likely induce NDRG1 by interacting with the oxygen-sensing pathway. |
Hypoxia mimetics treatment, HIF-1 knockout cells, Western blot, in vitro expression assays |
BMC genetics |
Medium |
15341671
|
| 2004 |
Nickel compounds induce HIF-1 transactivation and Cap43/NDRG1 protein expression through a PI3K/Akt-dependent and p70S6k-independent signaling pathway. |
Dominant-negative PI3K and Akt mutant overexpression, rapamycin inhibition, Western blot, HIF-1 transactivation assays |
Cancer research |
High |
14729612
|
| 2001 |
Ni(II) and Cu(II) bind to the C-terminal 10-amino acid repeat domain of Cap43/NDRG1 (sequence TRSRSHTSEG) via the imidazole nitrogen of histidine residues, forming octahedral and square planar complexes. |
pH-metric and spectroscopic analyses (UV-VIS, EPR, CD, NMR) of synthetic peptide |
Journal of inorganic biochemistry |
High |
11330481
|
| 2004 |
Ni(II) binds to two or three sites on the 20- and 30-amino acid C-terminal repeat fragments of Cap43/NDRG1 respectively, with each Ni(II) ion coordinated to the histidine imidazole of each 10-amino acid repeat unit. |
pH-metric titration, UV-visible spectroscopy, CD, NMR of synthetic peptide fragments |
Journal of inorganic biochemistry |
High |
15149799
|
| 2003 |
VHL tumor suppressor specifically downregulates Cap43/NDRG1 expression through an Sp1 site in the promoter region (−286 to −62 bp) of the Cap43 gene in renal cancer cells. |
VHL transfection into VHL-negative cells, Cap43 promoter deletion/mutation reporter assays, Western blot, Northern blot |
International journal of cancer |
High |
12767066
|
| 2013 |
NDRG1 binds and stabilizes MGMT (O6-methylguanine-DNA methyltransferase), conferring resistance to alkylating chemotherapy. NDRG1 is an mTORC2/SGK1 pathway target induced by hypoxia, irradiation, corticosteroids, and alkylating agents. |
Co-immunoprecipitation (NDRG1-MGMT interaction), NDRG1 knockdown/overexpression, mTORC2/SGK1 pathway analysis, patient tissue analysis |
Proceedings of the National Academy of Sciences of the United States of America |
High |
24367102
|
| 2009 |
NDRG1/Cap43 suppresses NF-κB signaling by decreasing IKKβ expression, reducing IκBα phosphorylation, and blocking nuclear translocation of p65/p50, thereby attenuating expression of CXC chemokines (CXCL1, CXCL5, IL-8) and VEGF-A; exogenous IKKβ rescues these effects. |
Stable overexpression, IKKβ rescue transfection, NF-κB reporter assays, ChIP, immunoblot, xenograft mouse models |
Cancer research |
High |
19491262
|
| 2010 |
Phosphorylation of NDRG1/Cap43 by SGK1 at both Ser330 and Thr346 (but not individually) in the C-terminal domain (aa 326–394) is required for suppression of NF-κB signaling and CXC chemokine (CXCL1, CXCL5) expression in pancreatic cancer cells. |
Deletion constructs, site-directed mutagenesis of Ser/Thr residues, stable expression, ELISA for chemokines, IκBα phosphorylation assays |
Biochemical and biophysical research communications |
High |
20416281
|
| 2011 |
NDRG1 is phosphorylated by SGK1 and GSK3β in a cell-cycle-dependent manner; phosphorylated NDRG1 co-localizes with γ-tubulin at centromeres and at the cleavage furrow during cytokinesis, suggesting a role in mitosis. |
Cell cycle synchronization (aphidicolin, nocodazole), immunofluorescence co-localization with γ-tubulin, p53-proficient vs. deficient HCT116 cells, phospho-specific antibodies |
Biochemical and biophysical research communications |
Medium |
21708134
|
| 2013 |
NDRG1 silencing in epithelial cells reduces LDL receptor (LDLR) abundance at the plasma membrane by causing LDLR accumulation in enlarged EEA1-positive endosomes with increased LDLR ubiquitylation; co-depletion of IDOL (E3 ligase) rescues LDLR at the plasma membrane, identifying NDRG1 as a regulator of multivesicular body formation and endosomal LDLR trafficking. |
siRNA silencing, confocal microscopy, LDLR ubiquitylation assays, co-depletion (NDRG1 + IDOL), LDL uptake assays, murine oligodendrocyte studies |
Journal of cell science |
High |
23813961
|
| 2005 |
NDRG1 physically interacts with apolipoproteins A-I and A-II (confirmed by yeast two-hybrid and mammalian cell co-immunoprecipitation), suggesting a role in Schwann cell lipid/cholesterol trafficking; the HMSNL founder mutation R148X is associated with decreased HDL-C levels. |
Yeast two-hybrid screening, reciprocal co-immunoprecipitation in mammalian cells, biochemical lipid analysis |
Biochemical and biophysical research communications |
Medium |
15922294
|
| 2011 |
NDRG1 promotes metastasis suppression through the ATF3/NF-κB/KAI1 transcriptional cascade: NDRG1 expression suppresses ATF3, which normally represses KAI1 through ATF3-NFκB co-repressor complex. Knockdown of KAI1 abrogates NDRG1-mediated metastasis suppression in vitro and in vivo. |
ChIP analysis of ATF3 binding to KAI1 promoter, stable NDRG1 overexpression/silencing, KAI1 promoter reporter assays, in vivo spontaneous metastasis animal model, immunohistochemistry |
The Journal of biological chemistry |
High |
21454613
|
| 2015 |
NDRG1 physically associates with γ-tubulin (centrosome component) and regulates centrosome number and amplification downstream of p53 in low-proliferative states; NDRG1 loss leads to centrosome amplification and genomic instability. |
Co-immunoprecipitation (NDRG1-γ-tubulin), RNAi and overexpression in isogenic TP53 WT/null/mutant cells, centrosome counting, genomic analysis |
Proceedings of the National Academy of Sciences of the United States of America |
High |
26324937
|
| 2015 |
NDRG1 is post-translationally modified by SUMO-2 predominantly at Lys14; SUMO-2 modification influences NDRG1 protein stability (a SUMO-2 fused NDRG1 K14R mutant shows dramatically decreased stability) without affecting subcellular distribution. SUMO-2-fused NDRG1 K14R also downregulates p21 expression. |
SUMO modification assays, NDRG1 mutant (K14R) construction, protein stability assays, subcellular fractionation, Western blot |
Biochemical and biophysical research communications |
Medium |
25712528
|
| 2015 |
Ndrg1 is an anergy factor in T cells induced by the transcription factor Egr2; Ndrg1 is phosphorylated and degraded via the proteasome upon CD28 costimulation and IL-2 treatment; Ndrg1-deficient T cells fail to become anergic and show hyperresponsiveness. |
Ndrg1 knockout mice, Ndrg1 overexpression, proteasome inhibitor treatment, T-cell anergy induction assays, autoimmune inflammation models |
Nature communications |
High |
26507712
|
| 2007 |
NDRG1 deficiency in mice impairs mast cell maturation and degranulation: Ndrg1-knockout mast cells show defective exocytosis (degranulation) after FcεRI crosslinking under CTMC-like maturation conditions, while leukotriene and cytokine production are unaffected. |
Ndrg1 knockout mouse, ex vivo bone marrow-derived mast cell (BMMC) co-culture with fibroblasts, FcεRI crosslinking assay, IgE-mediated anaphylaxis models |
Journal of immunology |
High |
17513753
|
| 2006 |
17β-estradiol (E2) decreases Cap43/NDRG1 expression dose-dependently through an estrogen receptor-α (ERα)-dependent pathway; overexpression of ERα in ER-negative cell lines is sufficient to downregulate Cap43, and anti-estrogens reverse this effect. |
Real-time PCR, immunoblotting, ERα cDNA transfection in ER-negative lines, anti-estrogen (tamoxifen, ICI 182780) treatment |
Clinical cancer research |
Medium |
16707596
|
| 2007 |
p53-dependent NDRG1 expression (induced by polyamine depletion) inhibits intestinal epithelial cell proliferation (DNA synthesis and cell number) without inducing apoptosis; NDRG1 overexpression inhibits growth regardless of endogenous p53, and p53-binding sites in the NDRG1 proximal promoter mediate this induction. |
p53 siRNA, p53 knockout cells, NDRG1 promoter deletion analysis, ectopic ODC overexpression, DNA synthesis assay, flow cytometry, TNF-α/cycloheximide apoptosis assay |
American journal of physiology. Cell physiology |
High |
17442733
|
| 2013 |
HIF-1α binds directly to the NDRG1 promoter (critical region −1202 to −450) to activate NDRG1 expression, and NDRG1 overexpression promotes proliferation and reduces apoptosis in A549 lung cancer cells. |
Promoter cloning and reporter assay, HIF-1α CDS overexpression, stable NDRG1 transfection, MTT assay, colony formation, flow cytometry |
Molecular biology reports |
Medium |
23526365
|
| 2013 |
SGK1 phosphorylates NDRG1 at serine/threonine sites; phospho-NDRG1 is increased in Alzheimer's disease brain tissue (~2-fold), suggesting augmented SGK1 activity targeting NDRG1 in AD. |
Immunoblot with phospho-specific NDRG1 antibody (SGK1-specific target), human post-mortem brain tissue analysis |
Neuropathology and applied neurobiology |
Low |
23363009
|
| 2017 |
NDRG1 inhibits EGFR/HER2 and HER2/HER3 heterodimer formation and promotes EGFR degradation, thereby attenuating ErbB oncogenic signaling. |
Co-immunoprecipitation, NDRG1 overexpression/knockdown, receptor dimerization assays, Western blot for receptor degradation |
The Journal of biological chemistry |
Medium |
28615452
|
| 2019 |
GSK3β phosphorylates serine and threonine residues in the C-terminal domain of NDRG1 and reduces NDRG1 protein stability. Conversely, NDRG1 overexpression decreases GSK3β levels via proteasomal degradation and suppresses AKT/S6 and cell-cycle signaling, revealing a bidirectional regulatory loop. |
GSK3β inhibitor treatment, NDRG1 overexpression/knockdown, proteasome inhibitor assays, Western blot for pathway targets, in vivo xenograft models |
Cancer research |
Medium |
31723002
|
| 2021 |
NDRG1 promotes interaction of the androgen receptor (AR) with chaperone HSP90, stabilizing AR while decreasing its androgen-mediated activation; NDRG1 also suppresses AR transcriptional activity partly by inhibiting c-Jun-AR interaction via reduced c-Jun phosphorylation. The CAP domain of NDRG1 is identified as vital for inhibition of AR activity. |
Co-immunoprecipitation (AR-HSP90), NDRG1 overexpression/knockdown, CAP-domain deletion mutants, AR transcriptional reporter assay, PSA expression analysis |
The Journal of biological chemistry |
High |
34785213
|
| 2021 |
Crystal structure of the α/β hydrolase domain of human NDRG1 was determined (PDB: 6ZMM); full-length NDRG1 has a flexible N- and C-terminal region; NDRG1 binds to lipid vesicles with conformational changes in the C-terminal region; NDRG1 interacts with metal ions (e.g., nickel) but aggregates in their presence. |
X-ray crystallography (PDB 6ZMM), small-angle X-ray scattering (SAXS), CD spectroscopy, lipid vesicle binding assays |
The FEBS journal |
High |
33305529
|
| 2017 |
NDRG1 loss disrupts the binding between RhoGDIα and CDC42, triggering CDC42 activation and downstream PAK1/Cofilin signaling, promoting filopodia formation and colorectal cancer invasiveness. |
NDRG1 silencing/overexpression, CDC42 activity assay (pull-down), Co-IP (RhoGDIα-CDC42), Western blot for PAK1/Cofilin, in vivo metastasis model |
International journal of biological sciences |
Medium |
33994856
|
| 2017 |
NDRG1 deficiency reduces active RhoA and Rac1 GTPases while upregulating active Cdc42; NDRG1-deficient prostate cancer cells have restricted actin dynamics (measured by fluorescent polymerized-actin sensor), reduced integrin expression and adhesion, increased EMMPRIN expression with altered glycosylation, increased matrix metalloproteases, and collective invasion phenotype. |
NDRG1 KD, Rho GTPase activity assays, live-cell fluorescent actin imaging (FRAP), EMMPRIN glycosylation analysis, 3D invasion assay, in vivo xenograft metastasis assay |
Molecular oncology |
High |
28371345
|
| 2021 |
NDRG1 enhances cetuximab (EGFR antibody) sensitivity in colorectal cancer by reducing EGFR expression, blocking EGFR phosphorylation, reducing EGFR at the cell membrane, and attenuating endocytosis/degradation of EGFR induced by caveolin-1 (Cav1). |
NDRG1 overexpression/knockdown, EGFR distribution analysis (membrane/cytoplasm/nuclear fractions), caveolin-1 co-immunoprecipitation, in vivo xenograft and patient tissue |
Oncogene |
Medium |
34385595
|
| 2020 |
NDRG1 forms a complex with PLCγ1 through its phosphorylation sites and is required for VEGF-A-induced PLCγ1 and ERK1/2 activation in endothelial cells; Ndrg1-knockout mice display impaired VEGF-A-induced corneal angiogenesis and reduced aortic sprouting. |
Co-immunoprecipitation (NDRG1-PLCγ1), Ndrg1 knockout mice, corneal angiogenesis assay, aortic ring sprouting assay, Western blot for PLCγ1/ERK activation, dorsal air sac assay |
Communications biology |
High |
32144393
|
| 2022 |
NDRG1 interacts with the orphan nuclear receptor Nur77 and functionally inhibits Nur77 transcriptional activity and NF-κB activity in endothelial cells; NDRG1 knockdown attenuates cytokine-induced MAPK activation, c-Jun phosphorylation, and AP-1 transcriptional activity. Endothelial cell-specific NDRG1 knockout mice show reduced neointima formation, atherosclerosis, and arterial thrombosis. |
Co-immunoprecipitation (NDRG1-Nur77), lentiviral shRNA knockdown, endothelial-specific NDRG1 KO mice, carotid artery ligation model, Nur77/NF-κB reporter assays, Western blot |
Circulation research |
High |
36562299
|
| 2023 |
Fasting or lipid availability activates mTORC2, which phosphorylates NDRG1 at Ser336; phosphorylated NDRG1 engages mitochondria and facilitates mitochondrial fission by cooperating with CDC42 and its effectors/regulators. The phosphorylation-deficient NDRG1-Ser336Ala mutant fails to support fission. |
Time-lapse imaging of NDRG1-mitochondria interaction, phospho-deficient mutant (NDRG1-S336A), siRNA screen, epistasis with DRP1-KO cells, proteomics, CDC42 co-immunoprecipitation, RictorKO and Cdc42-KO phenotyping |
Nature cell biology |
High |
37386153
|
| 2019 |
NDRG1 directly interacts with MIG6 (a tumor suppressor/EGFR regulator) and regulates c-Cbl E3 ligase activity as part of its mechanism for inhibiting receptor tyrosine kinases. |
Co-immunoprecipitation (NDRG1-MIG6), NDRG1 overexpression studies |
Cells |
Low |
34572031
|
| 2017 |
MNK1 (but not MNK2) signaling regulates NDRG1 phosphorylation; however, MNK1 cannot directly phosphorylate NDRG1 in vitro, indicating an indirect mechanism. MNK inhibition increases NDRG1 protein and mRNA expression. SGK1 phosphorylates MNK1 at a conserved site to repress its activity. |
MNK1/2 knockout cells, in vitro kinase assay (MNK1 vs. NDRG1), MNK inhibitors, SGK1 kinase assay on MNK1, Western blot |
Oncotarget |
Medium |
28545025
|
| 2019 |
NDRG1 regulates all three main arms of the ER stress response: increases ER chaperone expression (BiP, calreticulin, calnexin), suppresses PERK and IRE1α arms, and increases ATF6 cleavage. In the presence of anti-cancer agent Dp44mT, NDRG1 markedly increases eIF2α activation, maintains ATF4, elevates cytosolic Ca2+, and increases pro-apoptotic CHOP. |
NDRG1 overexpression/knockdown in pancreatic and colon cancer cells, Western blot for ER stress markers, Ca2+ measurement, confocal microscopy |
Biochimica et biophysica acta. Molecular basis of disease |
Medium |
30981813
|
| 2019 |
NDRG1 facilitates KSHV genome replication and episome persistence by interacting directly with PCNA (proliferating cell nuclear antigen) and forming a ternary complex with LANA (viral latent protein) and PCNA, bridging LANA to PCNA at viral terminal repeats (TRs) to facilitate viral DNA replication. |
Co-immunoprecipitation (NDRG1-PCNA, LANA-NDRG1-PCNA complex), NDRG1 knockdown in KSHV-infected cells, viral genome copy number assay, chromatin immunoprecipitation of PCNA at viral TRs |
PLoS pathogens |
High |
30811506
|
| 2020 |
NDRG1 suppresses autophagy at both the initiation stage and autolysosome formation (reducing LC3-LAMP2 co-localization, increasing p62); NDRG1 expression decreases cholesterol levels (independent of AMPK), sensitizing lysosomes to membrane permeabilization. |
NDRG1 overexpression/knockdown, confocal microscopy (LC3/LAMP2 co-localization), p62 Western blot, cholesterol determination, acridine orange staining for LMP, AMPK phosphorylation assays |
Biochimica et biophysica acta. General subjects |
Medium |
32335136
|
| 2018 |
NDRG1 regulates neutral lipid metabolism and lipid droplet formation in breast cancer cells; NDRG1 silencing increases fatty acid incorporation into neutral lipids and lipid droplets, while NDRG1 expression minimizes lipid droplet formation under both nutrient-replete and starvation conditions. |
NDRG1 silencing/overexpression, comprehensive lipidomics mass spectrometry, labeled fatty acid tracking, high-throughput quantitative microscopy, multiple breast cancer cell lines |
Breast cancer research |
High |
29898756
|
| 2017 |
Ndrg1 promotes adipocyte differentiation by inducing PPARγ expression and is required for C/EBPα phosphorylation; SGK1-dependent phosphorylation of Ndrg1 is induced during adipogenesis and promotes adipocyte formation. |
Ndrg1 knockdown/overexpression in adipocyte precursor cells, PPARγ and C/EBPα Western blot, adipogenesis differentiation assay |
Scientific reports |
Medium |
28775290
|
| 2024 |
NSUN6-mediated m5C methylation of NDRG1 mRNA enhances its stability via the m5C reader ALYREF; elevated NDRG1 expression promotes homologous recombination-mediated DNA repair, contributing to radioresistance in cervical cancer. |
Integrated m5C sequencing, mRNA sequencing, RNA immunoprecipitation, NSUN6 overexpression/silencing, CDX and 3D PDO models, in vivo xenograft |
Molecular cancer |
High |
38970106
|
| 2021 |
c-Jun, AR (androgen receptor), and DNMT1 form a complex at TRE regions of the NDRG1 promoter and suppress NDRG1 transcription through DNA hypermethylation; N-cadherin promotes c-Jun expression to suppress NDRG1, establishing an N-cadherin/c-Jun/NDRG1 axis in prostate cancer progression. |
Co-immunoprecipitation (c-Jun/AR/DNMT1 complex), ChIP at NDRG1 promoter TRE region, bisulfite sequencing for promoter methylation, NDRG1 knockdown/overexpression, in vivo xenograft |
International journal of biological sciences |
Medium |
34512147
|
| 2022 |
KDM1A (LSD1) histone demethylase represses NDRG1 expression; de-repression of NDRG1 by KDM1A inhibition causes inhibition of Wnt signaling and G1 cell cycle arrest in gastric cancer patient-derived organoids. |
CRISPR/Cas9 viability screen in patient-derived organoids, KDM1A genetic and pharmacological inhibition, NDRG1 expression measurement, cell cycle analysis, Wnt signaling assays |
Small methods |
Medium |
36908010
|
| 2022 |
Ndrg1a in zebrafish binds to the sodium-potassium ATPase (NKA) pump under anoxia and is required for NKA degradation, preserving ATP in kidney and ionocytes during hypoxia; sodium azide (which increases lactate) triggers NKA degradation in an Ndrg1a-dependent manner. |
Ndrg1a knockout zebrafish, co-immunoprecipitation (Ndrg1a-NKA), sodium azide treatment, anoxia survival assays, kidney function assays |
eLife |
High |
36214665
|
| 2023 |
MAOA interacts with NDRG1 and together they regulate glycolysis (Warburg effect) through suppression of the PI3K/AKT/mTOR pathway in gastric cancer. |
Co-immunoprecipitation (MAOA-NDRG1), Seahorse assay for glycolysis, Western blot for PI3K/AKT/mTOR pathway, overexpression/knockdown studies |
Cellular oncology |
Low |
37249744
|
| 2018 |
HER4 interacts with NDRG1 in osteosarcoma cells; NDRG1 overexpression antagonizes HER4 knockdown-mediated cell growth inhibition and apoptosis under stress conditions. |
Co-immunoprecipitation (HER4-NDRG1), shRNA knockdown of HER4, NDRG1 overexpression rescue assay, immunohistochemistry |
Biochimica et biophysica acta. Molecular basis of disease |
Low |
29524631
|
| 2024 |
NDRG1 inhibits ATG9A-dependent lysosomal-autophagy degradation of MHC class I (MHC-1) in pancreatic ductal adenocarcinoma cells, maintaining MHC-1 surface expression; elevated NDRG1 promotes CD8+ T cell infiltration and overcomes immune checkpoint blockade resistance. |
NDRG1 knockdown/overexpression, autophagy inhibitor studies, co-immunoprecipitation (NDRG1-ATG9A pathway), flow cytometry for MHC-1 and T cells, in vivo orthotopic mouse models, multiplex immunofluorescence |
Drug resistance updates |
Medium |
38228036
|
| 2025 |
NDRG1 stabilizes LDHA by inhibiting its ubiquitination, thereby enhancing glycolysis and promoting lactate accumulation in lung adenocarcinoma; histone H2B K58 lactylation at the NDRG1 locus (mediated by LDHA-generated lactate) represents an epigenetic feedback mechanism. |
NDRG1 knockdown/overexpression, ubiquitination assay (LDHA ubiquitylation), Seahorse glycolysis assay, lactate measurement, histone lactylation ChIP |
Advanced science |
Medium |
40539245
|
| 2016 |
NDRG1 physically associates with TLE2 and β-catenin to activate Wnt/β-catenin signaling in esophageal squamous cell carcinoma, promoting EMT; TLE2 overexpression prevents NDRG1-driven Wnt pathway activation. |
Co-immunoprecipitation (NDRG1-TLE2, NDRG1-β-catenin), stable lentiviral overexpression, RNAi, TLE2 overexpression epistasis, Western blot for EMT markers |
Cancer biology & therapy |
Low |
27414086
|
| 2020 |
NDRG1 binds directly to PI3K (co-immunoprecipitation) in placental JEG-3 cells; NDRG1 knockdown upregulates PI3K and AKT expression, identifying PI3K/AKT as a downstream mechanism of NDRG1-mediated suppression of angiogenesis. |
Co-immunoprecipitation (NDRG1-PI3K), lentiviral NDRG1 overexpression/knockdown, ELISA for PLGF/sFlt-1, Western blot for PI3K/AKT/VEGF, tube formation assay |
Pregnancy hypertension |
Low |
32470876
|
| 2022 |
In triple-negative breast cancer, YAP1 positively regulates NDRG1 transcription by binding the NDRG1 promoter; HJURP affects YAP1 ubiquitination and degradation, thereby modulating NDRG1 expression via the HJURP/YAP1/NDRG1 axis. |
YAP1 ChIP at NDRG1 promoter, ubiquitination assay (YAP1), HJURP knockdown/overexpression, Western blot, cell proliferation and chemosensitivity assays |
Cell death & disease |
Medium |
35459269
|
| 2011 |
NDRG1/Cap43 overexpression in hepatocellular carcinoma cells induces G0/G1 cell cycle arrest accompanied by increased p21 and decreased CDK4 expression both in vitro and in vivo. |
Stable NDRG1 transfection, cell cycle analysis (flow cytometry), Western blot for p21/CDK4, in vivo xenograft tumor growth, mimosine-induced G0/G1 block |
Cancer letters |
Medium |
21775055
|
| 2009 |
NDRG1 regulates endothelial cell migration under intermittent hypoxia: siRNA silencing of NDRG1 decreases endothelial cell migration under intermittent hypoxia (as identified by 2D-DIGE proteomics and confirmed by siRNA). |
2D-DIGE proteomics, mass spectrometry protein identification, siRNA knockdown, endothelial cell migration assay |
Angiogenesis |
Low |
19760510
|
| 2022 |
PTK7 (a membrane-localized pseudokinase) interacts with and stabilizes NDRG1 adjacent to adherens junctions; downregulation of either PTK7 or NDRG1 eliminates AZD9291 resistance in NSCLC cells. |
BioID proximal labeling (BirA*-PTK7), Co-immunoprecipitation (PTK7-NDRG1), knockdown/overexpression, phospho- and proximal proteomics |
ACS chemical biology |
Medium |
36205702
|