Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.73 (urokinase-type plasminogen activator)
10,685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship between the level of urokinase-type plasminogen activator (uPA) and pelvic lymph node metastasis was investigated in 20 patients with invasive cervical cancer of the uterus. Frozen sections from all surgical specimens were stained immunohistochemically by alkaline phosphatase anti-alkaline phosphatase method to detect uPA in cancer tissue. The concentration of uPA, determined immunologically, and the fibrinolytic activity were also examined in supernatants of homogenates of some cancer tissues. uPA was detected immunohistochemically in cancer cells of all specimens. A significant correlation was found between the extent of immunohistochemical staining for uPA and the concentration of uPA determined immunologically in cancer tissues (P less than 0.05). A positive correlation was also found between semiquantitative values determined by immunohistochemical staining for uPA and lymph node metastasis (P less than 0.05). Fibrinolytic activity in cancer tissues was confirmed by casein-plaque assay. These findings indicate that the pro-uPA/uPA contents in cervical cancer tissues are clinically useful for predicting the metastatic potential of these cancers to the pelvic lymph nodes.
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PMID:Clinical significance of urokinase-type plasminogen activator (uPA) in invasive cervical cancer of the uterus. 152 11

Overexpression of extracellular matrix metalloproteinase inducer (EMMPRIN) accelerates tumor invasion and metastasis via activation of matrix metalloproteinases (MMPs) and urokinase-type plasminogen activator (uPA) expression. The authors were interested in whether the scFv-M6-1B9 intrabody against EMMPRIN that retains EMMPRIN in endoplasmic reticulum could be a potential tool to suppress cervical cancer invasion through inhibition of uPA. The chimeric adenoviral vector Ad5/F35-scFv-M6-1B9 was transferred into human cervical carcinoma HeLa cells to produce the scFv-M6-1B9 intrabody against EMMPRIN. Cell surface expression of EMMPRIN, the membrane-bound uPA, the enzymatic activity of secreted uPA, and the invasion ability were analyzed. The scFv-M6-1B9 intrabody successfully diminished the cell surface expression of EMMPRIN and the membrane-bound uPA on HeLa cells. uPA activity from tissue culture media of EMMPRIN-downregulated HeLa cells was decreased. The invasion ability of HeLa cells harboring scFv-M6-1B9 intrabody was also suppressed. These results suggested that the scFv-M6-1B9 intrabody might represent a potential approach for invasive cervical cancer treatment. The application of scFv-M6-1B9 intrabody in animal experiments and preclinical studies would be investigated further.
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PMID:Downregulation of Extracellular Matrix Metalloproteinase Inducer by scFv-M6-1B9 Intrabody Suppresses Cervical Cancer Invasion Through Inhibition of Urokinase-Type Plasminogen Activator. 2811 37