ADAM15 Supports Prostate Cancer Metastasis by Modulating Tumor Cell–Endothelial Cell Interaction

• Published in: Cancer research (Chicago, Ill.) Vol. 68; no. 4; pp. 1092 - 1099
• Main Authors: Najy, Abdo J., Day, Kathleen C., Day, Mark L.
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Association for Cancer Research 15.02.2008
• Subjects: ADAM Proteins - biosynthesis; ADAM Proteins - genetics; ADAM Proteins - physiology; Animals; Antineoplastic agents; Biological and medical sciences; Bone Neoplasms - secondary; Cell Adhesion - physiology; Cell Communication - physiology; Cell Movement - physiology; Endothelial Cells - metabolism; Endothelial Cells - pathology; Gynecology. Andrology. Obstetrics; Humans; Hyaluronan Receptors - metabolism; Male; Male genital diseases; Matrix Metalloproteinase 9 - metabolism; Medical sciences; Membrane Proteins - biosynthesis; Membrane Proteins - genetics; Membrane Proteins - physiology; Mice; Mice, SCID; Neoplasm Metastasis; Nephrology. Urinary tract diseases; Pharmacology. Drug treatments; Prostatic Neoplasms - genetics; Prostatic Neoplasms - metabolism; Prostatic Neoplasms - pathology; RNA, Small Interfering - genetics; Tumors; Tumors of the urinary system; Urinary tract. Prostate gland; Endothelial cell; Urinary system disease; Prostate disease; Prostate metastasis; Cell cell interaction; Malignant tumor; Male genital diseases; Prostate cancer; Tumor cell; Cancer; Endothelium

Using human tumor and cDNA microarray technology, we have recently shown that the ADAM15 disintegrin is significantly overexpressed during the metastatic progression of human prostate cancer. In the current study, we used lentiviral-based short hairpin RNA (shRNA) technology to down-regulate ADAM15...