EC Number   |
Application |
Reference |
|---|
   3.4.24.B9 | medicine |
aberrant overexpression of ADAM9 is found in both gastric cancer tissues and cell lines. The expression of ADAM9 is significantly correlated with patient clinicopathological features including tumor size, local invasion, lymph node metastasis and tumor-node-metastasis stage. Knockdown of ADAM9 in gastric cancer SGC-7901 cells, which present the highest ADAM9 expression among the cell lines, induces a dramatic suppression of cell proliferation along with the arrest of the cell cycle in the G0/G1 phase. The 3' untranslated region of ADAM9 mRNA may be bound by miR-126, a suppressor in gastric cancer. Overexpression of miR-126 significantly downregulates ADAM9 in the gastric cancer cells |
754948 |
| 3.4.24.B9 | medicine |
ADAM9 enhances the expression of the pro-migratory protein CDCP1 to promote lung metastasis. Endogenous miR-218, which is abundant in normal lung tissue but suppressed in lung tumors, is regulated during the process of ADAM9-mediated CDCP1 expression. Suppression of miR-218 is associated with high migration ability in lung cancer cells |
755410 |
| 3.4.24.B9 | medicine |
ADAM9 staining is increased in lung epithelial cells and macrophages in smokers and even more so in patients with chronic obstructive pulmonary disease COPD. ADAM9 staining correlates directly with pack-year smoking history and inversely with airflow obstruction and/or FEV1 percent predicted. Bronchial epithelial cell ADAM9 mRNA levels are higher in patients with COPD than control subjects and correlate directly with pack-year smoking history |
752452 |
| 3.4.24.B9 | medicine |
all three enzymes ADAM9, ADAM12, and ADAM15 are significantly upregulated in gastric cancer compared to non-neoplastic foveolar epithelium. Anti-ADAM9 and anti-ADAM15 antibodies inhibit cell growth |
668997 |
| 3.4.24.B9 | medicine |
cells lacking ADAM9 show a significant reduction in infection efficiency by encephalomyocarditis virus EMCV. Pharmacological inhibition of the metalloproteinase activity of ADAM9 does not affect virus infection. Reconstitution of inactive ADAM9 in knockout cells restores susceptibility to EMCV. ADAM9 facilitates attachment of EMCV to the cell surface |
754597 |
| 3.4.24.B9 | medicine |
elevated level of enzyme in malignant compared to benign prostate tissue. Increase in enzyme protein and mRNA upon exposure of prostate cells to stress conditions. Inhibition of stress-induction of enzyme by actinomycin D and cycloheximide. Decrease of enzyme expression results in apoptotic cell death in prostate cancer cells |
668164 |
| 3.4.24.B9 | medicine |
enzyme overexpression in A-549 and EBC-1 cells results in increased invasive capacity in response to nerve growth factor, increased adhesion to brain tissue, and increased expression of integrin alpha3 and beta1 subunits. Administration of enzyme overexpressing A-549 cells to mice results in micrometastatic foci in brain and multiple metastatic colonies in the lungs |
668145 |
| 3.4.24.B9 | medicine |
in melanoma, enzyme expression is restricted to the melanoma cells within the invading front. Enzyme is detected in melanoma cells and in peritumoral stromal fibroblasts, but absent in fibroblasts distal to the tumor site. In melanoma cell lines, enzyme is expressed in varying amounts in all cell lines studied. Downregulation of enzyme expression upon culture of cells within 3-dimensional latticies of fibrillar type I collagen, but not in the polysaccharide alginate |
668979 |
| 3.4.24.B9 | medicine |
injection of murine melanoma cells into the flank of ADAM-9-/- animals resultsin the development of significantly larger tumors than in wild-type animals as a result of increased proliferation and decreased apoptosis of melanoma cells |
734427 |
| 3.4.24.B9 | medicine |
lung cancer cell line EBC-1, enzyme mRNA levels are significantly higher in highly brain-metastatic sublines than in the parent or highly bone-metastatic sublines |
668145 |
