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Disease on EC 3.4.24.B9 - ADAM9 endopeptidase

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DISEASE
TITLE OF PUBLICATION
LINK TO PUBMED
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
ADAM-9 expression in intestinal-type adenocarcinoma of the sinonasal tract.
ADAM9 contributes to vascular invasion in pancreatic ductal adenocarcinoma.
ADAM9 expression in pancreatic cancer is associated with tumour type and is a prognostic factor in ductal adenocarcinoma.
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
The pleiotropic roles of ADAM9 in the biology of solid tumors.
Adenocarcinoma of Lung
ADAM9 expression promotes an aggressive lung adenocarcinoma phenotype.
ADAM9 Up-Regulates N-Cadherin via miR-218 Suppression in Lung Adenocarcinoma Cells.
MicroRNA-425 promotes the development of lung adenocarcinoma via targeting A disintegrin and metalloproteinases 9 (ADAM9).
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.
Estrogen induced the expression of ADAM9 through estrogen receptor ? but not estrogen receptor ? in cultured human neuronal cells.
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.
Asthma
Expression of ADAMs and their inhibitors in sputum from patients with asthma.
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.
Increased expression of disintegrin-metalloproteinases ADAM-15 and ADAM-9 following upregulation of integrins alpha5beta1 and alphavbeta3 in atherosclerosis.
Blister
Gene expression profiling in dermatitis herpetiformis skin lesions.
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.
ADAM9 inhibition increases membrane activity of ADAM10 and controls ?-secretase processing of amyloid precursor protein.
ADAM9 Mediates Triple-Negative Breast Cancer Progression via AKT/NF-?B Pathway.
ADAM9 silencing inhibits breast tumor cell invasion in vitro.
Adam9 silencing inhibits breast tumor cells transmigration through blood and lymphatic endothelial cells.
Coexpression and coregulation analysis of time-series gene expression data in estrogen-induced breast cancer cell.
Expression of ADAM-9 mRNA and protein in human breast cancer.
Expression of Concern: microRNA-1298 inhibits the malignant behaviors of breast cancer cells via targeting ADAM9.
How ADAM-9 and ADAM-11 differentially from estrogen receptor predict response to tamoxifen treatment in patients with recurrent breast cancer: a retrospective study.
Increased expression of ADAM family members in human breast cancer and breast cancer cell lines.
Inhibition of platelets and tumor cell adhesion by the disintegrin domain of human ADAM9 to collagen I under dynamic flow conditions.
microRNA-1298 inhibits the malignant behaviors of breast cancer cells via targeting ADAM9.
MicroRNA-154/ADAM9 axis inhibits the proliferation, migration and invasion of breast cancer cells.
MiR-126 regulated breast cancer cell invasion by targeting ADAM9.
MiR-33a suppresses breast cancer cell proliferation and metastasis by targeting ADAM9 and ROS1.
Secreted and membrane-bound isoforms of protease ADAM9 have opposing effects on breast cancer cell migration.
The pleiotropic roles of ADAM9 in the biology of solid tumors.
[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 as a potential target molecule in cancer.
ADAM9 promotes lung cancer progression through vascular remodeling by VEGFA, ANGPT2, and PLAT.
Changes in expressions of ADAM9, 10, and 17 as well as ?-secretase activity in renal cell carcinoma.
Critical function for ADAM9 in mouse prostate cancer.
Gene expression profiles of microdissected pancreatic ductal adenocarcinoma.
Increased abundance of ADAM9 transcripts in the blood is associated with tissue damage.
microRNA-590 suppresses the tumorigenesis and invasiveness of non-small cell lung cancer cells by targeting ADAM9.
Overexpression of ADAM9 decreases radiosensitivity of hepatocellular carcinoma cell by activating autophagy.
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.
ADAM12 in human liver cancers: TGF-beta-regulated expression in stellate cells is associated with matrix remodeling.
ADAM9 expression in pancreatic cancer is associated with tumour type and is a prognostic factor in ductal adenocarcinoma.
ADAM9 is over-expressed in human ovarian clear cell carcinomas and suppresses cisplatin-induced cell death.
Adam9 silencing inhibits breast tumor cells transmigration through blood and lymphatic endothelial cells.
Changes in expressions of ADAM9, 10, and 17 as well as ?-secretase activity in renal cell carcinoma.
Critical function for ADAM9 in mouse prostate cancer.
Expression of ADAM-9 mRNA and protein in human breast cancer.
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
Fisetin Suppresses the Proliferation and Metastasis of Renal Cell Carcinoma through Upregulation of MEK/ERK-Targeting CTSS and ADAM9.
Genome wide analysis of chromosomal alterations in oral squamous cell carcinomas revealed over expression of MGAM and ADAM9.
Immunohistochemical and molecular profiling of histologically defined apocrine carcinomas of the breast.
MicroRNA-30a suppresses the proliferation, migration and invasion of human renal cell carcinoma cells by directly targeting ADAM9.
MiR-126 inhibits cell migration and invasion by targeting ADAM9 in oral squamous cell carcinoma.
Overexpression of ADAM9 in oral squamous cell carcinoma.
Overexpression of ADAM9 Promotes Colon Cancer Cells Invasion.
Oxidative and osmotic stress signaling in tumor cells is mediated by ADAM proteases and heparin-binding epidermal growth factor.
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.
ADAM9 mediates the interleukin-6-induced Epithelial-Mesenchymal transition and metastasis through ROS production in hepatoma cells.
Loss of tumor suppressor miR-126 contributes to the development of hepatitis B virus-related hepatocellular carcinoma metastasis through the upregulation of ADAM9.
miR-203 suppresses the proliferation and metastasis of hepatocellular carcinoma by targeting oncogene ADAM9 and oncogenic long non-coding RNA HULC.
MiR-488 suppresses cell proliferation and invasion by targeting ADAM9 and lncRNA HULC in hepatocellular carcinoma [Retraction].
MiR-488 suppresses cell proliferation and invasion by targeting ADAM9 and lncRNA HULC in hepatocellular carcinoma.
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.
Combined RNAi targeting human Stat3 and ADAM9 as gene therapy for non-small cell lung cancer.
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
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.
High expression of a disintegrin and metalloproteinase-9 predicts a shortened survival time in completely resected stage I non-small cell lung cancer.
microRNA-590 suppresses the tumorigenesis and invasiveness of non-small cell lung cancer cells by targeting ADAM9.
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.
Changes in expressions of ADAM9, 10, and 17 as well as ?-secretase activity in renal cell carcinoma.
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
Fisetin Suppresses the Proliferation and Metastasis of Renal Cell Carcinoma through Upregulation of MEK/ERK-Targeting CTSS and ADAM9.
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
Downregulated expression of ADAM9 in anterior polar cataracts.
Identification and functional clustering of global gene expression differences between human age-related cataract and clear lenses.
Novel ADAM9 homozygous mutation in a consanguineous Egyptian family with severe cone-rod dystrophy and cataract.
Choroidal Neovascularization
ADAM9 is involved in pathological retinal neovascularization.
Colonic Neoplasms
Overexpression of ADAM9 enhances growth factor-mediated recycling of E-cadherin in human colon cancer cell line HT29 cells.
Overexpression of ADAM9 Promotes Colon Cancer Cells Invasion.
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.
Exome sequencing reveals ADAM9 mutations in a child with cone-rod dystrophy.
Generalized progressive retinal atrophy in the Irish Glen of Imaal Terrier is associated with a deletion in the ADAM9 gene.
Loss of the metalloprotease ADAM9 leads to cone-rod dystrophy in humans and retinal degeneration in mice.
Novel ADAM9 homozygous mutation in a consanguineous Egyptian family with severe cone-rod dystrophy and cataract.
Novel retinopathy in related Gordon setters: a clinical, behavioral, electrophysiological, and genetic investigation.
Corneal Neovascularization
When MT1-MMP meets ADAMs.
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.
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.
Fibroadenoma
Expression of ADAM-9 mRNA and protein in human breast cancer.
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.
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.
Fisetin suppresses ADAM9 expression and inhibits invasion of glioma cancer cells through increased phosphorylation of ERK1/2.
Galangin increases ERK1/2 phosphorylation to decrease ADAM9 expression and prevents invasion in A172 glioma cells.
Licochalcone A inhibits the invasive potential of human glioma cells by targeting the MEK/ERK and ADAM9 signaling pathways.
MicroRNA-140 represses glioma growth and metastasis by directly targeting ADAM9.
The emerging role of the MiR-1272-ADAM9-CDCP1 signaling pathway in the progression of glioma.
The pleiotropic roles of ADAM9 in the biology of solid tumors.
Ubiquitin-specific peptidase 39 promotes human glioma cells migration and invasion by facilitating ADAM9 mRNA maturation.
Hearing Loss
ADAM9: A novel player in vestibular schwannoma pathogenesis.
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.
Encephalomyocarditis Virus Entry Unveiled.
Identification of the Cell-Surface Protease ADAM9 as an Entry Factor for Encephalomyocarditis Virus.
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.
The pleiotropic roles of ADAM9 in the biology of solid tumors.
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.
ADAM9 expression promotes an aggressive lung adenocarcinoma phenotype.
ADAM9 promotes lung cancer metastases to brain by a plasminogen activator-based pathway.
ADAM9 promotes lung cancer progression through vascular remodeling by VEGFA, ANGPT2, and PLAT.
ADAM9 Up-Regulates N-Cadherin via miR-218 Suppression in Lung Adenocarcinoma Cells.
Circular RNA circ_0020123 promotes non-small cell lung cancer progression by acting as a ceRNA for miR-488-3p to regulate ADAM9 expression.
Combined RNAi targeting human Stat3 and ADAM9 as gene therapy for non-small cell lung cancer.
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
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.
High expression of a disintegrin and metalloproteinase-9 predicts a shortened survival time in completely resected stage I non-small cell lung cancer.
microRNA-590 suppresses the tumorigenesis and invasiveness of non-small cell lung cancer cells by targeting ADAM9.
mir-126-5p Promotes Cisplatin Sensitivity of Non-Small-Cell Lung Cancer by Inhibiting ADAM9.
Overexpression of ADAM9 in non-small cell lung cancer correlates with brain metastasis.
Quercetin suppresses the metastatic ability of lung cancer through inhibiting Snail-dependent Akt activation and Snail-independent ADAM9 expression pathways.
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.
[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
Adam-9 expression and regulation in human skin melanoma and melanoma cell lines.
Deletion of ADAM-9 in HGF/CDK4 mice impairs melanoma development and metastasis.
Loss of ADAM9 Leads to Modifications of the Extracellular Matrix Modulating Tumor Growth.
miR-126&126* Restored Expressions Play a Tumor Suppressor Role by Directly Regulating ADAM9 and MMP7 in Melanoma.
miR-126-3p down-regulation contributes to dabrafenib acquired resistance in melanoma by up-regulating ADAM9 and VEGF-A.
Stromal Fibroblast-Specific Expression of ADAM-9 Modulates Proliferation and Apoptosis in Melanoma Cells In Vitro and In Vivo.
The disintegrin-like and cysteine-rich domains of ADAM-9 mediate interactions between melanoma cells and fibroblasts.
The pleiotropic roles of ADAM9 in the biology of solid tumors.
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.
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.
Aberrant expression of ADAM9 in ovarian cancer and its clinical significance.
ADAM12 in human liver cancers: TGF-beta-regulated expression in stellate cells is associated with matrix remodeling.
ADAM9 enhances CDCP1 by inhibiting miR-1 through EGFR signaling activation in lung cancer metastasis.
ADAM9 enhances CDCP1 protein expression by suppressing miR-218 for lung tumor metastasis.
ADAM9 Expression in Uterine Cervical Cancer and Its Associated Factors
ADAM9 expression promotes an aggressive lung adenocarcinoma phenotype.
ADAM9 functions as a promoter of gastric cancer growth which is negatively and post-transcriptionally regulated by miR-126.
ADAM9 is highly expressed in renal cell cancer and is associated with tumour progression.
ADAM9 mediates the interleukin-6-induced Epithelial-Mesenchymal transition and metastasis through ROS production in hepatoma cells.
ADAM9 promotes lung cancer metastases to brain by a plasminogen activator-based pathway.
ADAM9 silencing inhibits breast tumor cell invasion in vitro.
ADAM9 Up-Regulates N-Cadherin via miR-218 Suppression in Lung Adenocarcinoma Cells.
An Overview of ADAM9: Structure, Activation, and Regulation in Human Diseases.
Both macrophages and hypoxia play critical role in regulating invasion of gastric cancer in vitro.
Deletion of ADAM-9 in HGF/CDK4 mice impairs melanoma development and metastasis.
Depletion of hsa_circ_0000144 Suppresses Oxaliplatin Resistance of Gastric Cancer Cells by Regulating miR-502-5p/ADAM9 Axis.
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
Fisetin Suppresses the Proliferation and Metastasis of Renal Cell Carcinoma through Upregulation of MEK/ERK-Targeting CTSS and ADAM9.
In vivo targeting of ADAM9 gene expression using lentivirus-delivered shRNA suppresses prostate cancer growth by regulating REG4 dependent cell cycle progression.
KRAS/NF-?B/YY1/miR-489 Signaling Axis Controls Pancreatic Cancer Metastasis.
Loss of tumor suppressor miR-126 contributes to the development of hepatitis B virus-related hepatocellular carcinoma metastasis through the upregulation of ADAM9.
MicroRNA-126 inhibits proliferation and metastasis in prostate cancer via regulation of ADAM9.
MicroRNA-140 represses glioma growth and metastasis by directly targeting ADAM9.
miR-126 inhibits cell growth, invasion, and migration of osteosarcoma cells by downregulating ADAM-9.
miR-126-3p down-regulation contributes to dabrafenib acquired resistance in melanoma by up-regulating ADAM9 and VEGF-A.
miR-203 suppresses the proliferation and metastasis of hepatocellular carcinoma by targeting oncogene ADAM9 and oncogenic long non-coding RNA HULC.
MiR-33a suppresses breast cancer cell proliferation and metastasis by targeting ADAM9 and ROS1.
MiRNA-488-3p inhibits malignant progression of NSCLC by modulating ADAM9.
Overexpression of ADAM9 in non-small cell lung cancer correlates with brain metastasis.
Platelet integrin
Resveratrol-mediated ADAM9 degradation decreases cancer progression and provides synergistic effects in combination with chemotherapy.
RNAi-mediated A disintegrin and metalloproteinase 9 gene silencing inhibits the tumor growth of non-small lung cancer in vitro and in vivo.
RNAi-mediated ADAM9 gene silencing inhibits metastasis of adenoid cystic carcinoma cells.
Structure, regulatory factors and cancer-related physiological effects of ADAM9.
The pleiotropic roles of ADAM9 in the biology of solid tumors.
Tumor invasion induced by oxidative stress is dependent on membrane ADAM 9 protein and its secreted form.
[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.
A disintegrin and metalloproteinase 9 is involved in ectodomain shedding of receptor-binding cancer antigen expressed on SiSo cells.
A secreted form of ADAM9 promotes carcinoma invasion through tumor-stromal interactions.
Aberrant expression of ADAM9 in ovarian cancer and its clinical significance.
Activation of epidermal growth factor receptor signaling by the prostaglandin E(2) receptor EP4 pathway during gastric tumorigenesis.
ADAM-17 expression is enhanced by FoxM1 and is a poor prognostic sign in gastric carcinoma.
ADAM-17 is a poor prognostic indicator for patients with hilar cholangiocarcinoma and is regulated by FoxM1.
Adam-9 expression and regulation in human skin melanoma and melanoma cell lines.
ADAM12 in human liver cancers: TGF-beta-regulated expression in stellate cells is associated with matrix remodeling.
ADAM9 as a potential target molecule in cancer.
ADAM9 contributes to vascular invasion in pancreatic ductal adenocarcinoma.
ADAM9 disintegrin domain activates human neutrophils through an autocrine circuit involving integrins and CXCR2.
ADAM9 enhances CDCP1 protein expression by suppressing miR-218 for lung tumor metastasis.
ADAM9 expression in pancreatic cancer is associated with tumour type and is a prognostic factor in ductal adenocarcinoma.
ADAM9 Expression in Uterine Cervical Cancer and Its Associated Factors
ADAM9 expression is a significant and independent prognostic marker of PSA relapse in prostate cancer.
ADAM9 Expression Is Associate with Glioma Tumor Grade and Histological Type, and Acts as a Prognostic Factor in Lower-Grade Gliomas.
ADAM9 expression promotes an aggressive lung adenocarcinoma phenotype.
ADAM9 functions as a promoter of gastric cancer growth which is negatively and post-transcriptionally regulated by miR-126.
ADAM9 is highly expressed in renal cell cancer and is associated with tumour progression.
ADAM9 is involved in pathological retinal neovascularization.
ADAM9 promotes lung cancer metastases to brain by a plasminogen activator-based pathway.
ADAM9 silencing inhibits breast tumor cell invasion in vitro.
Adam9 silencing inhibits breast tumor cells transmigration through blood and lymphatic endothelial cells.
ADAM9: A novel player in vestibular schwannoma pathogenesis.
ADAMs family members as amyloid precursor protein alpha-secretases.
ADAMs in cancer cell proliferation and progression.
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.
Amplicons in breast cancers analyzed by multiplex ligation-dependent probe amplification and fluorescence In Situ hybridization.
An Overview of ADAM9: Structure, Activation, and Regulation in Human Diseases.
Both macrophages and hypoxia play critical role in regulating invasion of gastric cancer in vitro.
Cancer-associated fibroblast stimulates cancer cell invasion in an interleukin-1 receptor (IL-1R)-dependent manner.
Characterization of the Catalytic Properties of the Membrane-anchored Metalloprotease ADAM9 in Cell-based assays.
Cloning and expression in Pichia pastoris of metalloprotease domain of ADAM 9 catalytically active against fibronectin.
Combined Dynamic Alterations in Urinary VEGF Levels and Tissue ADAM9 Expression as Markers for Lethal Phenotypic Progression of Prostate Cancer.
Critical function for ADAM9 in mouse prostate cancer.
Developmental expression of metalloproteases ADAM 9, 10, and 17 becomes restricted to divergent pancreatic compartments.
Expression of ADAM-9 mRNA and protein in human breast cancer.
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
Expression of ADAMs (a disintegrin and metalloproteases) and TIMP-3 (tissue inhibitor of metalloproteinase-3) in human prostatic adenocarcinomas.
Expression of CD133 confers malignant potential by regulating metalloproteinases in human hepatocellular carcinoma.
Fisetin suppresses ADAM9 expression and inhibits invasion of glioma cancer cells through increased phosphorylation of ERK1/2.
Galangin increases ERK1/2 phosphorylation to decrease ADAM9 expression and prevents invasion in A172 glioma cells.
Gene expression profiles of microdissected pancreatic ductal adenocarcinoma.
How ADAM-9 and ADAM-11 differentially from estrogen receptor predict response to tamoxifen treatment in patients with recurrent breast cancer: a retrospective study.
Identification of tumor antigens and immune subtypes of pancreatic adenocarcinoma for mRNA vaccine development.
In vivo targeting of ADAM9 gene expression using lentivirus-delivered shRNA suppresses prostate cancer growth by regulating REG4 dependent cell cycle progression.
Increased abundance of ADAM9 transcripts in the blood is associated with tissue damage.
Increased expression of ADAM 9 and ADAM 15 mRNA in pancreatic cancer.
Inhibition of platelets and tumor cell adhesion by the disintegrin domain of human ADAM9 to collagen I under dynamic flow conditions.
Long Non-coding RNA RUNDC3A-AS1 Promotes Lung Metastasis of Thyroid Cancer via Targeting the miR-182-5p/ADAM9.
Loss of ADAM9 expression impairs ?1 integrin endocytosis, focal adhesion formation and cancer cell migration.
Loss of ADAM9 Leads to Modifications of the Extracellular Matrix Modulating Tumor Growth.
Loss of miR-126 is crucial to pancreatic cancer progression.
Loss of tumor suppressor miR-126 contributes to the development of hepatitis B virus-related hepatocellular carcinoma metastasis through the upregulation of ADAM9.
MicroRNA-1274a serves as a prognostic biomarker in patients with osteosarcoma and is involved in tumor progression via targeting ADAM9.
MicroRNA-140 represses glioma growth and metastasis by directly targeting ADAM9.
MicroRNA-154/ADAM9 axis inhibits the proliferation, migration and invasion of breast cancer cells.
microRNA-520f reverses epithelial-to-mesenchymal transition by targeting ADAM9 and TGFBR2.
microRNA-590 suppresses the tumorigenesis and invasiveness of non-small cell lung cancer cells by targeting ADAM9.
MicroRNA?543 inhibits proliferation, invasion and induces apoptosis of glioblastoma cells by directly targeting ADAM9.
MiR-126 acts as a tumor suppressor in pancreatic cancer cells via the regulation of ADAM9.
miR-126 in human cancers: clinical roles and current perspectives.
miR-126 inhibits cell growth, invasion, and migration of osteosarcoma cells by downregulating ADAM-9.
MiR-126 regulated breast cancer cell invasion by targeting ADAM9.
miR-126&126* Restored Expressions Play a Tumor Suppressor Role by Directly Regulating ADAM9 and MMP7 in Melanoma.
mir-126-5p Promotes Cisplatin Sensitivity of Non-Small-Cell Lung Cancer by Inhibiting ADAM9.
MiR-129-5p functions as a tumor suppressor in gastric cancer progression through targeting ADAM9.
miR-203 suppresses the proliferation and metastasis of hepatocellular carcinoma by targeting oncogene ADAM9 and oncogenic long non-coding RNA HULC.
Platelet integrin
Recombinant disintegrin domain of human ADAM9 inhibits migration and invasion of DU145 prostate tumor cells.
Resveratrol-mediated ADAM9 degradation decreases cancer progression and provides synergistic effects in combination with chemotherapy.
Retinoids Decrease Soluble MICA Concentration by Inhibiting the Enzymatic Activity of ADAM9 and ADAM10.
RNAi-mediated A disintegrin and metalloproteinase 9 gene silencing inhibits the tumor growth of non-small lung cancer in vitro and in vivo.
RNAi-mediated ADAM9 gene silencing inhibits metastasis of adenoid cystic carcinoma cells.
Role of ADAMs in cancer formation and progression.
Sp1-mediated microRNA-182 expression regulates lung cancer progression.
Stromal Fibroblast-Specific Expression of ADAM-9 Modulates Proliferation and Apoptosis in Melanoma Cells In Vitro and In Vivo.
Structure, regulatory factors and cancer-related physiological effects of ADAM9.
Tetraspanin CD9 interacts with ?-secretase to enhance its oncogenic function in pancreatic cancer.
The ADAMs family of proteases: new biomarkers and therapeutic targets for cancer?
The disintegrin-like and cysteine-rich domains of ADAM-9 mediate interactions between melanoma cells and fibroblasts.
The disintegrin-metalloproteinases ADAM9, ADAM12, and ADAM15 are upregulated in gastric cancer.
The effect of disintegrin-metalloproteinase ADAM9 in gastric cancer progression.
The pleiotropic roles of ADAM9 in the biology of solid tumors.
The role of ADAMs in disease pathophysiology.
Tumor invasion induced by oxidative stress is dependent on membrane ADAM 9 protein and its secreted form.
Neurofibromatoses
ADAM9: A novel player in vestibular schwannoma pathogenesis.
Neurofibromatosis 2
ADAM9: A novel player in vestibular schwannoma pathogenesis.
Neuroma, Acoustic
ADAM9: A novel player in vestibular schwannoma pathogenesis.
Analysis of ADAM9 regulation and function in vestibular schwannoma primary cells.
Osteosarcoma
MicroRNA-126 Overexpression Inhibits Proliferation and Invasion in Osteosarcoma Cells.
MicroRNA-1274a serves as a prognostic biomarker in patients with osteosarcoma and is involved in tumor progression via targeting ADAM9.
MicroRNA?302a suppresses cell proliferation, migration and invasion in osteosarcoma by targeting ADAM9.
miR-126 inhibits cell growth, invasion, and migration of osteosarcoma cells by downregulating ADAM-9.
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.
Bone Marrow Mesenchymal Stem Cell-Derived Exosomal MicroRNA-126-3p Inhibits Pancreatic Cancer Development by Targeting ADAM9.
Circular RNA ADAM9 facilitates the malignant behaviours of pancreatic cancer by sponging miR-217 and upregulating PRSS3 expression.
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
Gene expression analysis of pancreatic cell lines reveals genes overexpressed in pancreatic cancer.
Increased expression of ADAM 9 and ADAM 15 mRNA in pancreatic cancer.
Loss of miR-126 is crucial to pancreatic cancer progression.
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.
Pre-Eclampsia
High altitude and pre-eclampsia: Adaptation or protection.
Prostatic Hyperplasia
Expression of ADAMs (a disintegrin and metalloproteases) and TIMP-3 (tissue inhibitor of metalloproteinase-3) in human prostatic adenocarcinomas.
Prostatic Intraepithelial Neoplasia
Critical function for ADAM9 in mouse prostate cancer.
Prostatic Neoplasms
ADAM9 decreases in castration resistant prostate cancer and is a prognostic factor for overall survival.
ADAM9 expression is a significant and independent prognostic marker of PSA relapse in prostate cancer.
Combined Dynamic Alterations in Urinary VEGF Levels and Tissue ADAM9 Expression as Markers for Lethal Phenotypic Progression of Prostate Cancer.
Critical function for ADAM9 in mouse prostate cancer.
Editorial comment on: ADAM9 expression is a significant and independent prognostic marker of PSA relapse in prostate cancer.
In vivo targeting of ADAM9 gene expression using lentivirus-delivered shRNA suppresses prostate cancer growth by regulating REG4 dependent cell cycle progression.
Inhibition of ADAM9 expression induces epithelial phenotypic alterations and sensitizes human prostate cancer cells to radiation and chemotherapy.
MicroRNA-126 inhibits proliferation and metastasis in prostate cancer via regulation of ADAM9.
Oxidative stress induces ADAM9 protein expression in human prostate cancer cells.
Reactive oxygen species mediate androgen receptor- and serum starvation-elicited downstream signaling of ADAM9 expression in human prostate cancer cells.
Stabilization of ADAM9 by N-?-acetyltransferase 10 protein contributes to promoting progression of androgen-independent prostate cancer.
The expression of the ADAMs proteases in prostate cancer cell lines and their regulation by dihydrotestosterone.
The pleiotropic roles of ADAM9 in the biology of solid tumors.
Pulmonary Disease, Chronic Obstructive
A Disintegrin and A Metalloproteinase-9 (ADAM9): A Novel Proteinase Culprit with Multifarious Contributions to COPD.
ADAM9: A Damaging Player in Chronic Obstructive Pulmonary Disease.
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.
Loss of the metalloprotease ADAM9 leads to cone-rod dystrophy in humans and retinal degeneration in mice.
Retinal Neovascularization
ADAM9 is involved in pathological 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.
MiR-126 inhibits cell migration and invasion by targeting ADAM9 in oral squamous cell carcinoma.
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.
ADAM17 promotes lymph node metastasis in gastric cancer via activation of the Notch and Wnt signaling pathways.
ADAM9 functions as a promoter of gastric cancer growth which is negatively and post-transcriptionally regulated by miR-126.
Both macrophages and hypoxia play critical role in regulating invasion of gastric cancer in vitro.
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
LncRNA LINC00689 Promotes the Progression of Gastric Cancer Through Upregulation of ADAM9 by Sponging miR-526b-3p.
Macrophage coculture enhanced invasion of gastric cancer cells via TGF-? and BMP pathways.
MiR-129-5p functions as a tumor suppressor in gastric cancer progression through targeting ADAM9.
The disintegrin-metalloproteinases ADAM9, ADAM12, and ADAM15 are upregulated in gastric cancer.
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
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.