Increased plasminogen activator and type IV collagenase activity in invasive follicular thyroid carcinoma cells.
Surgery
; 118(6): 1011-6; discussion 1016-7, 1995 Dec.
Article
em En
| MEDLINE
| ID: mdl-7491516
ABSTRACT
BACKGROUND:
An essential difference between benign and malignant follicular thyroid tumors is the ability to invade and metastasize. Thyrotropin (TSH) stimulates invasion of cultured human follicular thyroid cancer cells (FTC-133) via a protein kinase C (PKC) dependent mechanism. Tumor invasion depends on degradation of extracellular matrix by proteases.METHODS:
We analyzed protease activity in FTC-133 and its more invasive clone, FTC-238. Cells were treated with TSH or 12-0-tetradecanoyl-phorbol-13-acetate (TPA), a PKC agonist, for 24 hours. Conditioned medium and cellular extract were subjected to substrate gel zymography with either casein-plasminogen or gelatin (collagen). Western blot and immunohistochemistry confirmed protease identity.RESULTS:
We found increased 50 kd urokinase-like plasminogen activator (uPA) and 62 kd gelatinase activity by FTC-238 cells compared with the less invasive FTC-133 cells. There was no effect of TSH on uPA or collagenase activity at concentrations of 0.01 to 10 mU/ml. In both FTC-133 and FTC-238, TPA incubations of 0.1 to 100 ng/ml caused a dose-dependent increase in uPA and a 94 kd type IV collagenase.CONCLUSIONS:
These findings show that TSH-stimulated invasion may be due to PKC-induced activation of uPA and 94 kd type IV collagenase. uPA and basement membrane type IV collagenase warrant investigation as markers for follicular thyroid cancer.
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Base de dados:
MEDLINE
Assunto principal:
Neoplasias da Glândula Tireoide
/
Ativador de Plasminogênio Tipo Uroquinase
/
Adenoma
/
Colagenases
Limite:
Humans
Idioma:
En
Ano de publicação:
1995
Tipo de documento:
Article