Disease on EC 3.4.24.B9 - ADAM9 endopeptidase
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Acute Lung Injury
ADAM9 is a novel product of polymorphonuclear neutrophils: regulation of expression and contributions to extracellular matrix protein degradation during acute lung injury.
Adenocarcinoma
ADAM9 expression in pancreatic cancer is associated with tumour type and is a prognostic factor in ductal adenocarcinoma.
Adenocarcinoma
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
Adenocarcinoma of Lung
ADAM9 expression promotes an aggressive lung adenocarcinoma phenotype.
Adenocarcinoma of Lung
ADAM9 Up-Regulates N-Cadherin via miR-218 Suppression in Lung Adenocarcinoma Cells.
Adenocarcinoma of Lung
MicroRNA-425 promotes the development of lung adenocarcinoma via targeting A disintegrin and metalloproteinases 9 (ADAM9).
Adenocarcinoma of Lung
mir-126-5p Promotes Cisplatin Sensitivity of Non-Small-Cell Lung Cancer by Inhibiting ADAM9.
Alzheimer Disease
ADAM9 inhibition increases membrane activity of ADAM10 and controls ?-secretase processing of amyloid precursor protein.
Alzheimer Disease
Estrogen induced the expression of ADAM9 through estrogen receptor ? but not estrogen receptor ? in cultured human neuronal cells.
Alzheimer Disease
Promoter polymorphisms which regulate ADAM9 transcription are protective against sporadic Alzheimer's disease.
Aortic Aneurysm, Abdominal
Role of ADAM9 and miR-126 in the development of abdominal aortic aneurysm.
Atherosclerosis
ADAM-9, ADAM-15, and ADAM-17 are upregulated in macrophages in advanced human atherosclerotic plaques in aorta and carotid and femoral arteries--Tampere vascular study.
Atherosclerosis
Increased expression of disintegrin-metalloproteinases ADAM-15 and ADAM-9 following upregulation of integrins alpha5beta1 and alphavbeta3 in atherosclerosis.
Brain Neoplasms
ADAM9 promotes lung cancer metastases to brain by a plasminogen activator-based pathway.
Breast Neoplasms
ADAM22 as a prognostic and therapeutic drug target in the treatment of endocrine-resistant breast cancer.
Breast Neoplasms
ADAM9 inhibition increases membrane activity of ADAM10 and controls ?-secretase processing of amyloid precursor protein.
Breast Neoplasms
ADAM9 Mediates Triple-Negative Breast Cancer Progression via AKT/NF-?B Pathway.
Breast Neoplasms
Adam9 silencing inhibits breast tumor cells transmigration through blood and lymphatic endothelial cells.
Breast Neoplasms
Coexpression and coregulation analysis of time-series gene expression data in estrogen-induced breast cancer cell.
Breast Neoplasms
Expression of Concern: microRNA-1298 inhibits the malignant behaviors of breast cancer cells via targeting ADAM9.
Breast Neoplasms
How ADAM-9 and ADAM-11 differentially from estrogen receptor predict response to tamoxifen treatment in patients with recurrent breast cancer: a retrospective study.
Breast Neoplasms
Increased expression of ADAM family members in human breast cancer and breast cancer cell lines.
Breast Neoplasms
Inhibition of platelets and tumor cell adhesion by the disintegrin domain of human ADAM9 to collagen I under dynamic flow conditions.
Breast Neoplasms
microRNA-1298 inhibits the malignant behaviors of breast cancer cells via targeting ADAM9.
Breast Neoplasms
MicroRNA-154/ADAM9 axis inhibits the proliferation, migration and invasion of breast cancer cells.
Breast Neoplasms
MiR-33a suppresses breast cancer cell proliferation and metastasis by targeting ADAM9 and ROS1.
Breast Neoplasms
Secreted and membrane-bound isoforms of protease ADAM9 have opposing effects on breast cancer cell migration.
Breast Neoplasms
[Key gene leading to poor prognosis of triple-negative breast cancer based on bioinformatics analysis].
Breast Neoplasms, Male
Oncogene amplification in male breast cancer: analysis by multiplex ligation-dependent probe amplification.
Carcinogenesis
ADAM9 promotes lung cancer progression through vascular remodeling by VEGFA, ANGPT2, and PLAT.
Carcinogenesis
Changes in expressions of ADAM9, 10, and 17 as well as ?-secretase activity in renal cell carcinoma.
Carcinogenesis
Gene expression profiles of microdissected pancreatic ductal adenocarcinoma.
Carcinogenesis
Increased abundance of ADAM9 transcripts in the blood is associated with tissue damage.
Carcinogenesis
microRNA-590 suppresses the tumorigenesis and invasiveness of non-small cell lung cancer cells by targeting ADAM9.
Carcinogenesis
Overexpression of ADAM9 decreases radiosensitivity of hepatocellular carcinoma cell by activating autophagy.
Carcinogenesis
Tetraspanin CD9 interacts with ?-secretase to enhance its oncogenic function in pancreatic cancer.
Carcinoma
A secreted form of ADAM9 promotes carcinoma invasion through tumor-stromal interactions.
Carcinoma
ADAM12 in human liver cancers: TGF-beta-regulated expression in stellate cells is associated with matrix remodeling.
Carcinoma
ADAM9 expression in pancreatic cancer is associated with tumour type and is a prognostic factor in ductal adenocarcinoma.
Carcinoma
ADAM9 is over-expressed in human ovarian clear cell carcinomas and suppresses cisplatin-induced cell death.
Carcinoma
Adam9 silencing inhibits breast tumor cells transmigration through blood and lymphatic endothelial cells.
Carcinoma
Changes in expressions of ADAM9, 10, and 17 as well as ?-secretase activity in renal cell carcinoma.
Carcinoma
Fisetin Suppresses the Proliferation and Metastasis of Renal Cell Carcinoma through Upregulation of MEK/ERK-Targeting CTSS and ADAM9.
Carcinoma
Genome wide analysis of chromosomal alterations in oral squamous cell carcinomas revealed over expression of MGAM and ADAM9.
Carcinoma
Immunohistochemical and molecular profiling of histologically defined apocrine carcinomas of the breast.
Carcinoma
MicroRNA-30a suppresses the proliferation, migration and invasion of human renal cell carcinoma cells by directly targeting ADAM9.
Carcinoma
MiR-126 inhibits cell migration and invasion by targeting ADAM9 in oral squamous cell carcinoma.
Carcinoma
Oxidative and osmotic stress signaling in tumor cells is mediated by ADAM proteases and heparin-binding epidermal growth factor.
Carcinoma
RNAi-mediated ADAM9 gene silencing inhibits metastasis of adenoid cystic carcinoma cells.
Carcinoma, Acinar Cell
ADAM9 expression in pancreatic cancer is associated with tumour type and is a prognostic factor in ductal adenocarcinoma.
Carcinoma, Adenoid Cystic
RNAi-mediated ADAM9 gene silencing inhibits metastasis of adenoid cystic carcinoma cells.
Carcinoma, Hepatocellular
ADAM12 in human liver cancers: TGF-beta-regulated expression in stellate cells is associated with matrix remodeling.
Carcinoma, Hepatocellular
ADAM9 mediates the interleukin-6-induced Epithelial-Mesenchymal transition and metastasis through ROS production in hepatoma cells.
Carcinoma, Hepatocellular
Loss of tumor suppressor miR-126 contributes to the development of hepatitis B virus-related hepatocellular carcinoma metastasis through the upregulation of ADAM9.
Carcinoma, Hepatocellular
miR-203 suppresses the proliferation and metastasis of hepatocellular carcinoma by targeting oncogene ADAM9 and oncogenic long non-coding RNA HULC.
Carcinoma, Hepatocellular
MiR-488 suppresses cell proliferation and invasion by targeting ADAM9 and lncRNA HULC in hepatocellular carcinoma [Retraction].
Carcinoma, Hepatocellular
MiR-488 suppresses cell proliferation and invasion by targeting ADAM9 and lncRNA HULC in hepatocellular carcinoma.
Carcinoma, Hepatocellular
Overexpression of ADAM9 decreases radiosensitivity of hepatocellular carcinoma cell by activating autophagy.
Carcinoma, Intraductal, Noninfiltrating
Molecular differences between ductal carcinoma in situ and adjacent invasive breast carcinoma: A multiplex ligation-dependent probe amplification study.
Carcinoma, Non-Small-Cell Lung
Circular RNA circ_0020123 promotes non-small cell lung cancer progression by acting as a ceRNA for miR-488-3p to regulate ADAM9 expression.
Carcinoma, Non-Small-Cell Lung
Combined RNAi targeting human Stat3 and ADAM9 as gene therapy for non-small cell lung cancer.
Carcinoma, Non-Small-Cell Lung
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
Carcinoma, Non-Small-Cell Lung
HDGF and ADAM9 are novel molecular staging biomarkers, prognostic biomarkers and predictive biomarkers for adjuvant chemotherapy in surgically resected stage I non-small cell lung cancer.
Carcinoma, Non-Small-Cell Lung
High expression of a disintegrin and metalloproteinase-9 predicts a shortened survival time in completely resected stage I non-small cell lung cancer.
Carcinoma, Non-Small-Cell Lung
microRNA-590 suppresses the tumorigenesis and invasiveness of non-small cell lung cancer cells by targeting ADAM9.
Carcinoma, Non-Small-Cell Lung
Overexpression of ADAM9 in non-small cell lung cancer correlates with brain metastasis.
Carcinoma, Ovarian Epithelial
Circ_0005276 aggravates the development of epithelial ovarian cancer by targeting ADAM9.
Carcinoma, Renal Cell
ADAM9 is highly expressed in renal cell cancer and is associated with tumour progression.
Carcinoma, Renal Cell
Changes in expressions of ADAM9, 10, and 17 as well as ?-secretase activity in renal cell carcinoma.
Carcinoma, Renal Cell
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
Carcinoma, Renal Cell
Fisetin Suppresses the Proliferation and Metastasis of Renal Cell Carcinoma through Upregulation of MEK/ERK-Targeting CTSS and ADAM9.
Carcinoma, Renal Cell
MicroRNA-30a suppresses the proliferation, migration and invasion of human renal cell carcinoma cells by directly targeting ADAM9.
Carcinoma, Squamous Cell
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
Cardiomegaly
MiR-30e-5p is sponged by Kcnq1ot1 and represses Angiotensin II-induced hypertrophic phenotypes in cardiomyocytes by targeting ADAM9.
Cataract
Identification and functional clustering of global gene expression differences between human age-related cataract and clear lenses.
Cataract
Novel ADAM9 homozygous mutation in a consanguineous Egyptian family with severe cone-rod dystrophy and cataract.
Colonic Neoplasms
Overexpression of ADAM9 enhances growth factor-mediated recycling of E-cadherin in human colon cancer cell line HT29 cells.
Color Vision Defects
Novel retinopathy in related Gordon setters: a clinical, behavioral, electrophysiological, and genetic investigation.
Cone-Rod Dystrophies
An ADAM9 mutation in canine cone-rod dystrophy 3 establishes homology with human cone-rod dystrophy 9.
Cone-Rod Dystrophies
Exome sequencing reveals ADAM9 mutations in a child with cone-rod dystrophy.
Cone-Rod Dystrophies
Generalized progressive retinal atrophy in the Irish Glen of Imaal Terrier is associated with a deletion in the ADAM9 gene.
Cone-Rod Dystrophies
Loss of the metalloprotease ADAM9 leads to cone-rod dystrophy in humans and retinal degeneration in mice.
Cone-Rod Dystrophies
Novel ADAM9 homozygous mutation in a consanguineous Egyptian family with severe cone-rod dystrophy and cataract.
Cone-Rod Dystrophies
Novel retinopathy in related Gordon setters: a clinical, behavioral, electrophysiological, and genetic investigation.
Dermatomyositis
The cell-specific expression of metalloproteinase-disintegrins (ADAMs) in inflammatory myopathies.
Encephalitis
Identification of the Cell-Surface Protease ADAM9 as an Entry Factor for Encephalomyocarditis Virus.
Endometrial Neoplasms
A disintegrin and metalloproteinase 9 is involved in ectodomain shedding of receptor-binding cancer antigen expressed on SiSo cells.
Endometrial Neoplasms
Long non-coding RNA (lncRNA) HOXB-AS3 promotes cell proliferation and inhibits apoptosis by regulating ADAM9 expression through targeting miR-498-5p in endometrial carcinoma.
Esophageal Neoplasms
Resveratrol-mediated ADAM9 degradation decreases cancer progression and provides synergistic effects in combination with chemotherapy.
Esophagitis
Disintegrin and metalloproteinases (ADAMs) expression in gastroesophageal reflux disease and in esophageal adenocarcinoma.
Gastritis
ADAM proteases involved in inflammation are differentially altered in patients with gastritis or ulcer.
Glioblastoma
ADAM9 Expression Is Associate with Glioma Tumor Grade and Histological Type, and Acts as a Prognostic Factor in Lower-Grade Gliomas.
Glioblastoma
MicroRNA?543 inhibits proliferation, invasion and induces apoptosis of glioblastoma cells by directly targeting ADAM9.
Glioma
ADAM9 Expression Is Associate with Glioma Tumor Grade and Histological Type, and Acts as a Prognostic Factor in Lower-Grade Gliomas.
Glioma
Fisetin suppresses ADAM9 expression and inhibits invasion of glioma cancer cells through increased phosphorylation of ERK1/2.
Glioma
Galangin increases ERK1/2 phosphorylation to decrease ADAM9 expression and prevents invasion in A172 glioma cells.
Glioma
Licochalcone A inhibits the invasive potential of human glioma cells by targeting the MEK/ERK and ADAM9 signaling pathways.
Glioma
The emerging role of the MiR-1272-ADAM9-CDCP1 signaling pathway in the progression of glioma.
Glioma
Ubiquitin-specific peptidase 39 promotes human glioma cells migration and invasion by facilitating ADAM9 mRNA maturation.
Hepatitis B
Loss of tumor suppressor miR-126 contributes to the development of hepatitis B virus-related hepatocellular carcinoma metastasis through the upregulation of ADAM9.
Infections
A Disintegrin and Metalloproteinase 9 Domain (ADAM9) Is a Major Susceptibility Factor in the Early Stages of Encephalomyocarditis Virus Infection.
Infections
Identification of the Cell-Surface Protease ADAM9 as an Entry Factor for Encephalomyocarditis Virus.
Infections
Increased abundance of ADAM9 transcripts in the blood is associated with tissue damage.
Kidney Neoplasms
ADAM9 is highly expressed in renal cell cancer and is associated with tumour progression.
Klatskin Tumor
ADAM-17 is a poor prognostic indicator for patients with hilar cholangiocarcinoma and is regulated by FoxM1.
Liver Neoplasms
ADAM12 in human liver cancers: TGF-beta-regulated expression in stellate cells is associated with matrix remodeling.
Lung Injury
ADAM9 is a novel product of polymorphonuclear neutrophils: regulation of expression and contributions to extracellular matrix protein degradation during acute lung injury.
Lung Neoplasms
ADAM9 enhances CDCP1 by inhibiting miR-1 through EGFR signaling activation in lung cancer metastasis.
Lung Neoplasms
ADAM9 promotes lung cancer metastases to brain by a plasminogen activator-based pathway.
Lung Neoplasms
ADAM9 promotes lung cancer progression through vascular remodeling by VEGFA, ANGPT2, and PLAT.
Lung Neoplasms
ADAM9 Up-Regulates N-Cadherin via miR-218 Suppression in Lung Adenocarcinoma Cells.
Lung Neoplasms
Circular RNA circ_0020123 promotes non-small cell lung cancer progression by acting as a ceRNA for miR-488-3p to regulate ADAM9 expression.
Lung Neoplasms
Combined RNAi targeting human Stat3 and ADAM9 as gene therapy for non-small cell lung cancer.
Lung Neoplasms
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
Lung Neoplasms
HDGF and ADAM9 are novel molecular staging biomarkers, prognostic biomarkers and predictive biomarkers for adjuvant chemotherapy in surgically resected stage I non-small cell lung cancer.
Lung Neoplasms
High expression of a disintegrin and metalloproteinase-9 predicts a shortened survival time in completely resected stage I non-small cell lung cancer.
Lung Neoplasms
microRNA-590 suppresses the tumorigenesis and invasiveness of non-small cell lung cancer cells by targeting ADAM9.
Lung Neoplasms
mir-126-5p Promotes Cisplatin Sensitivity of Non-Small-Cell Lung Cancer by Inhibiting ADAM9.
Lung Neoplasms
Overexpression of ADAM9 in non-small cell lung cancer correlates with brain metastasis.
Lung Neoplasms
Quercetin suppresses the metastatic ability of lung cancer through inhibiting Snail-dependent Akt activation and Snail-independent ADAM9 expression pathways.
Lung Neoplasms
Resveratrol-mediated ADAM9 degradation decreases cancer progression and provides synergistic effects in combination with chemotherapy.
Lupus Erythematosus, Systemic
ADAM9 enhances Th17 cell differentiation and autoimmunity by activating TGF-?1.
Lymphatic Metastasis
ADAM9 functions as a promoter of gastric cancer growth which is negatively and post-transcriptionally regulated by miR-126.
Lymphatic Metastasis
[Key gene leading to poor prognosis of triple-negative breast cancer based on bioinformatics analysis].
Lymphoma
Amoeboid shape change and contact guidance: T-lymphocyte crawling through fibrillar collagen is independent of matrix remodeling by MMPs and other proteases.
Melanoma
Loss of ADAM9 Leads to Modifications of the Extracellular Matrix Modulating Tumor Growth.
Melanoma
miR-126&126* Restored Expressions Play a Tumor Suppressor Role by Directly Regulating ADAM9 and MMP7 in Melanoma.
Melanoma
miR-126-3p down-regulation contributes to dabrafenib acquired resistance in melanoma by up-regulating ADAM9 and VEGF-A.
Melanoma
Stromal Fibroblast-Specific Expression of ADAM-9 Modulates Proliferation and Apoptosis in Melanoma Cells In Vitro and In Vivo.
Melanoma
The disintegrin-like and cysteine-rich domains of ADAM-9 mediate interactions between melanoma cells and fibroblasts.
Melanoma
UV-induced EGFR signal transactivation is dependent on proligand shedding by activated metalloproteases in skin cancer cell lines.
Meningioma
Comparative gene expression profiling of ADAMs, MMPs, TIMPs, EMMPRIN, EGF-R and VEGFA in low grade meningioma.
Mouth Neoplasms
Involvement of the A disintegrin and metalloproteinase 9 in oral cancer cell invasion.
Multiple Myeloma
ADAM-9 (MDC-9/meltrin-gamma), a member of the a disintegrin and metalloproteinase family, regulates myeloma-cell-induced interleukin-6 production in osteoblasts by direct interaction with the alpha(v)beta5 integrin.
Myocarditis
A Disintegrin and Metalloproteinase 9 Domain (ADAM9) Is a Major Susceptibility Factor in the Early Stages of Encephalomyocarditis Virus Infection.
Myocarditis
Identification of the Cell-Surface Protease ADAM9 as an Entry Factor for Encephalomyocarditis Virus.
Myositis
The cell-specific expression of metalloproteinase-disintegrins (ADAMs) in inflammatory myopathies.
Myositis, Inclusion Body
The cell-specific expression of metalloproteinase-disintegrins (ADAMs) in inflammatory myopathies.
Neoplasm Metastasis
A secreted form of ADAM9 promotes carcinoma invasion through tumor-stromal interactions.
Neoplasm Metastasis
Aberrant expression of ADAM9 in ovarian cancer and its clinical significance.
Neoplasm Metastasis
ADAM12 in human liver cancers: TGF-beta-regulated expression in stellate cells is associated with matrix remodeling.
Neoplasm Metastasis
ADAM9 enhances CDCP1 by inhibiting miR-1 through EGFR signaling activation in lung cancer metastasis.
Neoplasm Metastasis
ADAM9 enhances CDCP1 protein expression by suppressing miR-218 for lung tumor metastasis.
Neoplasm Metastasis
ADAM9 functions as a promoter of gastric cancer growth which is negatively and post-transcriptionally regulated by miR-126.
Neoplasm Metastasis
ADAM9 is highly expressed in renal cell cancer and is associated with tumour progression.
Neoplasm Metastasis
ADAM9 mediates the interleukin-6-induced Epithelial-Mesenchymal transition and metastasis through ROS production in hepatoma cells.
Neoplasm Metastasis
ADAM9 promotes lung cancer metastases to brain by a plasminogen activator-based pathway.
Neoplasm Metastasis
ADAM9 Up-Regulates N-Cadherin via miR-218 Suppression in Lung Adenocarcinoma Cells.
Neoplasm Metastasis
An Overview of ADAM9: Structure, Activation, and Regulation in Human Diseases.
Neoplasm Metastasis
Both macrophages and hypoxia play critical role in regulating invasion of gastric cancer in vitro.
Neoplasm Metastasis
Deletion of ADAM-9 in HGF/CDK4 mice impairs melanoma development and metastasis.
Neoplasm Metastasis
Depletion of hsa_circ_0000144 Suppresses Oxaliplatin Resistance of Gastric Cancer Cells by Regulating miR-502-5p/ADAM9 Axis.
Neoplasm Metastasis
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
Neoplasm Metastasis
Fisetin Suppresses the Proliferation and Metastasis of Renal Cell Carcinoma through Upregulation of MEK/ERK-Targeting CTSS and ADAM9.
Neoplasm Metastasis
In vivo targeting of ADAM9 gene expression using lentivirus-delivered shRNA suppresses prostate cancer growth by regulating REG4 dependent cell cycle progression.
Neoplasm Metastasis
KRAS/NF-?B/YY1/miR-489 Signaling Axis Controls Pancreatic Cancer Metastasis.
Neoplasm Metastasis
Loss of tumor suppressor miR-126 contributes to the development of hepatitis B virus-related hepatocellular carcinoma metastasis through the upregulation of ADAM9.
Neoplasm Metastasis
MicroRNA-126 inhibits proliferation and metastasis in prostate cancer via regulation of ADAM9.
Neoplasm Metastasis
MicroRNA-140 represses glioma growth and metastasis by directly targeting ADAM9.
Neoplasm Metastasis
miR-126 inhibits cell growth, invasion, and migration of osteosarcoma cells by downregulating ADAM-9.
Neoplasm Metastasis
miR-126-3p down-regulation contributes to dabrafenib acquired resistance in melanoma by up-regulating ADAM9 and VEGF-A.
Neoplasm Metastasis
miR-203 suppresses the proliferation and metastasis of hepatocellular carcinoma by targeting oncogene ADAM9 and oncogenic long non-coding RNA HULC.
Neoplasm Metastasis
MiR-33a suppresses breast cancer cell proliferation and metastasis by targeting ADAM9 and ROS1.
Neoplasm Metastasis
MiRNA-488-3p inhibits malignant progression of NSCLC by modulating ADAM9.
Neoplasm Metastasis
Overexpression of ADAM9 in non-small cell lung cancer correlates with brain metastasis.
Neoplasm Metastasis
Resveratrol-mediated ADAM9 degradation decreases cancer progression and provides synergistic effects in combination with chemotherapy.
Neoplasm Metastasis
RNAi-mediated A disintegrin and metalloproteinase 9 gene silencing inhibits the tumor growth of non-small lung cancer in vitro and in vivo.
Neoplasm Metastasis
RNAi-mediated ADAM9 gene silencing inhibits metastasis of adenoid cystic carcinoma cells.
Neoplasm Metastasis
Structure, regulatory factors and cancer-related physiological effects of ADAM9.
Neoplasm Metastasis
Tumor invasion induced by oxidative stress is dependent on membrane ADAM 9 protein and its secreted form.
Neoplasm Metastasis
[Key gene leading to poor prognosis of triple-negative breast cancer based on bioinformatics analysis].
Neoplasms
A Disintegrin and Metalloproteinase 9 (ADAM9) in Advanced Hepatocellular Carcinoma and Their Role as a Biomarker During Hepatocellular Carcinoma Immunotherapy.
Neoplasms
A disintegrin and metalloproteinase 9 is involved in ectodomain shedding of receptor-binding cancer antigen expressed on SiSo cells.
Neoplasms
A secreted form of ADAM9 promotes carcinoma invasion through tumor-stromal interactions.
Neoplasms
Activation of epidermal growth factor receptor signaling by the prostaglandin E(2) receptor EP4 pathway during gastric tumorigenesis.
Neoplasms
ADAM-17 expression is enhanced by FoxM1 and is a poor prognostic sign in gastric carcinoma.
Neoplasms
ADAM-17 is a poor prognostic indicator for patients with hilar cholangiocarcinoma and is regulated by FoxM1.
Neoplasms
ADAM12 in human liver cancers: TGF-beta-regulated expression in stellate cells is associated with matrix remodeling.
Neoplasms
ADAM9 disintegrin domain activates human neutrophils through an autocrine circuit involving integrins and CXCR2.
Neoplasms
ADAM9 enhances CDCP1 protein expression by suppressing miR-218 for lung tumor metastasis.
Neoplasms
ADAM9 expression in pancreatic cancer is associated with tumour type and is a prognostic factor in ductal adenocarcinoma.
Neoplasms
ADAM9 expression is a significant and independent prognostic marker of PSA relapse in prostate cancer.
Neoplasms
ADAM9 Expression Is Associate with Glioma Tumor Grade and Histological Type, and Acts as a Prognostic Factor in Lower-Grade Gliomas.
Neoplasms
ADAM9 functions as a promoter of gastric cancer growth which is negatively and post-transcriptionally regulated by miR-126.
Neoplasms
ADAM9 is highly expressed in renal cell cancer and is associated with tumour progression.
Neoplasms
ADAM9 promotes lung cancer metastases to brain by a plasminogen activator-based pathway.
Neoplasms
Adam9 silencing inhibits breast tumor cells transmigration through blood and lymphatic endothelial cells.
Neoplasms
Age-Dependent Changes in the Pulmonary Renin-Angiotensin System Are Associated With Severity of Lung Injury in a Model of Acute Lung Injury in Rats.
Neoplasms
Amplicons in breast cancers analyzed by multiplex ligation-dependent probe amplification and fluorescence In Situ hybridization.
Neoplasms
Both macrophages and hypoxia play critical role in regulating invasion of gastric cancer in vitro.
Neoplasms
Cancer-associated fibroblast stimulates cancer cell invasion in an interleukin-1 receptor (IL-1R)-dependent manner.
Neoplasms
Characterization of the Catalytic Properties of the Membrane-anchored Metalloprotease ADAM9 in Cell-based assays.
Neoplasms
Cloning and expression in Pichia pastoris of metalloprotease domain of ADAM 9 catalytically active against fibronectin.
Neoplasms
Combined Dynamic Alterations in Urinary VEGF Levels and Tissue ADAM9 Expression as Markers for Lethal Phenotypic Progression of Prostate Cancer.
Neoplasms
Developmental expression of metalloproteases ADAM 9, 10, and 17 becomes restricted to divergent pancreatic compartments.
Neoplasms
Expression of ADAMs (a disintegrin and metalloproteases) and TIMP-3 (tissue inhibitor of metalloproteinase-3) in human prostatic adenocarcinomas.
Neoplasms
Expression of CD133 confers malignant potential by regulating metalloproteinases in human hepatocellular carcinoma.
Neoplasms
Fisetin suppresses ADAM9 expression and inhibits invasion of glioma cancer cells through increased phosphorylation of ERK1/2.
Neoplasms
Galangin increases ERK1/2 phosphorylation to decrease ADAM9 expression and prevents invasion in A172 glioma cells.
Neoplasms
How ADAM-9 and ADAM-11 differentially from estrogen receptor predict response to tamoxifen treatment in patients with recurrent breast cancer: a retrospective study.
Neoplasms
Identification of tumor antigens and immune subtypes of pancreatic adenocarcinoma for mRNA vaccine development.
Neoplasms
In vivo targeting of ADAM9 gene expression using lentivirus-delivered shRNA suppresses prostate cancer growth by regulating REG4 dependent cell cycle progression.
Neoplasms
Increased abundance of ADAM9 transcripts in the blood is associated with tissue damage.
Neoplasms
Inhibition of platelets and tumor cell adhesion by the disintegrin domain of human ADAM9 to collagen I under dynamic flow conditions.
Neoplasms
Long Non-coding RNA RUNDC3A-AS1 Promotes Lung Metastasis of Thyroid Cancer via Targeting the miR-182-5p/ADAM9.
Neoplasms
Loss of ADAM9 expression impairs ?1 integrin endocytosis, focal adhesion formation and cancer cell migration.
Neoplasms
Loss of ADAM9 Leads to Modifications of the Extracellular Matrix Modulating Tumor Growth.
Neoplasms
Loss of tumor suppressor miR-126 contributes to the development of hepatitis B virus-related hepatocellular carcinoma metastasis through the upregulation of ADAM9.
Neoplasms
MicroRNA-1274a serves as a prognostic biomarker in patients with osteosarcoma and is involved in tumor progression via targeting ADAM9.
Neoplasms
MicroRNA-154/ADAM9 axis inhibits the proliferation, migration and invasion of breast cancer cells.
Neoplasms
microRNA-520f reverses epithelial-to-mesenchymal transition by targeting ADAM9 and TGFBR2.
Neoplasms
microRNA-590 suppresses the tumorigenesis and invasiveness of non-small cell lung cancer cells by targeting ADAM9.
Neoplasms
MicroRNA?543 inhibits proliferation, invasion and induces apoptosis of glioblastoma cells by directly targeting ADAM9.
Neoplasms
MiR-126 acts as a tumor suppressor in pancreatic cancer cells via the regulation of ADAM9.
Neoplasms
miR-126 inhibits cell growth, invasion, and migration of osteosarcoma cells by downregulating ADAM-9.
Neoplasms
miR-126&126* Restored Expressions Play a Tumor Suppressor Role by Directly Regulating ADAM9 and MMP7 in Melanoma.
Neoplasms
mir-126-5p Promotes Cisplatin Sensitivity of Non-Small-Cell Lung Cancer by Inhibiting ADAM9.
Neoplasms
MiR-129-5p functions as a tumor suppressor in gastric cancer progression through targeting ADAM9.
Neoplasms
miR-203 suppresses the proliferation and metastasis of hepatocellular carcinoma by targeting oncogene ADAM9 and oncogenic long non-coding RNA HULC.
Neoplasms
Recombinant disintegrin domain of human ADAM9 inhibits migration and invasion of DU145 prostate tumor cells.
Neoplasms
Resveratrol-mediated ADAM9 degradation decreases cancer progression and provides synergistic effects in combination with chemotherapy.
Neoplasms
Retinoids Decrease Soluble MICA Concentration by Inhibiting the Enzymatic Activity of ADAM9 and ADAM10.
Neoplasms
RNAi-mediated A disintegrin and metalloproteinase 9 gene silencing inhibits the tumor growth of non-small lung cancer in vitro and in vivo.
Neoplasms
RNAi-mediated ADAM9 gene silencing inhibits metastasis of adenoid cystic carcinoma cells.
Neoplasms
Stromal Fibroblast-Specific Expression of ADAM-9 Modulates Proliferation and Apoptosis in Melanoma Cells In Vitro and In Vivo.
Neoplasms
Tetraspanin CD9 interacts with ?-secretase to enhance its oncogenic function in pancreatic cancer.
Neoplasms
The ADAMs family of proteases: new biomarkers and therapeutic targets for cancer?
Neoplasms
The disintegrin-like and cysteine-rich domains of ADAM-9 mediate interactions between melanoma cells and fibroblasts.
Neoplasms
The disintegrin-metalloproteinases ADAM9, ADAM12, and ADAM15 are upregulated in gastric cancer.
Neoplasms
Tumor invasion induced by oxidative stress is dependent on membrane ADAM 9 protein and its secreted form.
Neuroma, Acoustic
Analysis of ADAM9 regulation and function in vestibular schwannoma primary cells.
Osteosarcoma
MicroRNA-126 Overexpression Inhibits Proliferation and Invasion in Osteosarcoma Cells.
Osteosarcoma
MicroRNA-1274a serves as a prognostic biomarker in patients with osteosarcoma and is involved in tumor progression via targeting ADAM9.
Osteosarcoma
MicroRNA?302a suppresses cell proliferation, migration and invasion in osteosarcoma by targeting ADAM9.
Osteosarcoma
miR-126 inhibits cell growth, invasion, and migration of osteosarcoma cells by downregulating ADAM-9.
Osteosarcoma
Regulation of insulin-like growth factor binding protein-5, four and a half lim-2, and a disintegrin and metalloprotease-9 expression in osteoblasts.
Ovarian Neoplasms
Aberrant expression of ADAM9 in ovarian cancer and its clinical significance.
Pancreatic Neoplasms
ADAM9 expression in pancreatic cancer is associated with tumour type and is a prognostic factor in ductal adenocarcinoma.
Pancreatic Neoplasms
Bone Marrow Mesenchymal Stem Cell-Derived Exosomal MicroRNA-126-3p Inhibits Pancreatic Cancer Development by Targeting ADAM9.
Pancreatic Neoplasms
Circular RNA ADAM9 facilitates the malignant behaviours of pancreatic cancer by sponging miR-217 and upregulating PRSS3 expression.
Pancreatic Neoplasms
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
Pancreatic Neoplasms
Gene expression analysis of pancreatic cell lines reveals genes overexpressed in pancreatic cancer.
Pancreatic Neoplasms
MiR-126 acts as a tumor suppressor in pancreatic cancer cells via the regulation of ADAM9.
Pancreatitis, Chronic
ADAM9 expression in pancreatic cancer is associated with tumour type and is a prognostic factor in ductal adenocarcinoma.
Pneumonia
ADAM-family metalloproteinases in lung inflammation: potential therapeutic targets.
Polymyositis
The cell-specific expression of metalloproteinase-disintegrins (ADAMs) in inflammatory myopathies.
Prostatic Hyperplasia
Expression of ADAMs (a disintegrin and metalloproteases) and TIMP-3 (tissue inhibitor of metalloproteinase-3) in human prostatic adenocarcinomas.
Prostatic Neoplasms
ADAM9 decreases in castration resistant prostate cancer and is a prognostic factor for overall survival.
Prostatic Neoplasms
ADAM9 expression is a significant and independent prognostic marker of PSA relapse in prostate cancer.
Prostatic Neoplasms
Combined Dynamic Alterations in Urinary VEGF Levels and Tissue ADAM9 Expression as Markers for Lethal Phenotypic Progression of Prostate Cancer.
Prostatic Neoplasms
Editorial comment on: ADAM9 expression is a significant and independent prognostic marker of PSA relapse in prostate cancer.
Prostatic Neoplasms
In vivo targeting of ADAM9 gene expression using lentivirus-delivered shRNA suppresses prostate cancer growth by regulating REG4 dependent cell cycle progression.
Prostatic Neoplasms
Inhibition of ADAM9 expression induces epithelial phenotypic alterations and sensitizes human prostate cancer cells to radiation and chemotherapy.
Prostatic Neoplasms
MicroRNA-126 inhibits proliferation and metastasis in prostate cancer via regulation of ADAM9.
Prostatic Neoplasms
Oxidative stress induces ADAM9 protein expression in human prostate cancer cells.
Prostatic Neoplasms
Reactive oxygen species mediate androgen receptor- and serum starvation-elicited downstream signaling of ADAM9 expression in human prostate cancer cells.
Prostatic Neoplasms
Stabilization of ADAM9 by N-?-acetyltransferase 10 protein contributes to promoting progression of androgen-independent prostate cancer.
Prostatic Neoplasms
The expression of the ADAMs proteases in prostate cancer cell lines and their regulation by dihydrotestosterone.
Pulmonary Disease, Chronic Obstructive
A Disintegrin and A Metalloproteinase-9 (ADAM9): A Novel Proteinase Culprit with Multifarious Contributions to COPD.
Pulmonary Disease, Chronic Obstructive
ADAM9: A Damaging Player in Chronic Obstructive Pulmonary Disease.
Pulmonary Disease, Chronic Obstructive
Relationship Between Proteinase with a Disintegrin and a Metalloproteinase Domain-9 (ADAM9), Inflammation, Airway Remodeling, and Emphysema in COPD Patients.
Retinal Degeneration
Loss of the metalloprotease ADAM9 leads to cone-rod dystrophy in humans and retinal degeneration in mice.
Retinal Diseases
Generalized progressive retinal atrophy in the Irish Glen of Imaal Terrier is associated with a deletion in the ADAM9 gene.
Retinal Diseases
Loss of the metalloprotease ADAM9 leads to cone-rod dystrophy in humans and retinal degeneration in mice.
Retinal Neovascularization
Characterization of the Catalytic Properties of the Membrane-anchored Metalloprotease ADAM9 in Cell-based assays.
Squamous Cell Carcinoma of Head and Neck
Genome wide analysis of chromosomal alterations in oral squamous cell carcinomas revealed over expression of MGAM and ADAM9.
Squamous Cell Carcinoma of Head and Neck
MiR-126 inhibits cell migration and invasion by targeting ADAM9 in oral squamous cell carcinoma.
Squamous Cell Carcinoma of Head and Neck
Overexpression of ADAM9 in oral squamous cell carcinoma.
Starvation
Reactive oxygen species mediate androgen receptor- and serum starvation-elicited downstream signaling of ADAM9 expression in human prostate cancer cells.
Status Epilepticus
ADAM9, ADAM10, and ADAM15 mRNA levels in the rat brain after kainic acid-induced status epilepticus.
Stomach Neoplasms
ADAM-17 expression is enhanced by FoxM1 and is a poor prognostic sign in gastric carcinoma.
Stomach Neoplasms
ADAM17 promotes lymph node metastasis in gastric cancer via activation of the Notch and Wnt signaling pathways.
Stomach Neoplasms
ADAM9 functions as a promoter of gastric cancer growth which is negatively and post-transcriptionally regulated by miR-126.
Stomach Neoplasms
Both macrophages and hypoxia play critical role in regulating invasion of gastric cancer in vitro.
Stomach Neoplasms
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
Stomach Neoplasms
LncRNA LINC00689 Promotes the Progression of Gastric Cancer Through Upregulation of ADAM9 by Sponging miR-526b-3p.
Stomach Neoplasms
Macrophage coculture enhanced invasion of gastric cancer cells via TGF-? and BMP pathways.
Stomach Neoplasms
MiR-129-5p functions as a tumor suppressor in gastric cancer progression through targeting ADAM9.
Stomach Neoplasms
The disintegrin-metalloproteinases ADAM9, ADAM12, and ADAM15 are upregulated in gastric cancer.
Stomach Neoplasms
The effect of disintegrin-metalloproteinase ADAM9 in gastric cancer progression.
Thyroid Neoplasms
Long Non-coding RNA RUNDC3A-AS1 Promotes Lung Metastasis of Thyroid Cancer via Targeting the miR-182-5p/ADAM9.
Triple Negative Breast Neoplasms
ADAM9 Mediates Triple-Negative Breast Cancer Progression via AKT/NF-?B Pathway.
Urinary Bladder Neoplasms
MicroRNA-126 inhibits invasion in bladder cancer via regulation of ADAM9.
Uterine Cervical Neoplasms
ADAM9 Expression in Uterine Cervical Cancer and Its
Associated Factors
Uterine Cervical Neoplasms
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
Virus Diseases
Identification of the Cell-Surface Protease ADAM9 as an Entry Factor for Encephalomyocarditis Virus.
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