RESUMEN
Many carcinoma-associated markers are glycoconjugates whose expression undergoes temporal or spatial regulation. Mucin-1 (MUC1), discovered through monoclonal antibody technology, is a well-documented example of such a molecule and influences numerous pathophysiological behaviors, such as the invasion and metastasis of carcinoma cells. Levels of MUC1 expression in carcinomas correlate with the clinical stage of the cancer and inversely correlate with the survival prospects of patients. The MUC1 immune response is known to provide a protective host defense mechanism against cancer. The multiple functions of MUC1 in carcinoma-host interactions are believed to be dependent on the polymorphic nature of MUC1, particularly its glycosylation status.
Asunto(s)
Mucina-1/fisiología , Neoplasias/fisiopatología , Secuencia de Aminoácidos , Animales , Vacunas contra el Cáncer/farmacología , Comunicación Celular , Glicosilación , Humanos , Inmunoterapia , Modelos Biológicos , Datos de Secuencia Molecular , Mucina-1/química , Mucina-1/genética , Mucina-1/inmunología , Neoplasias/química , Neoplasias/inmunología , Polimorfismo Genético , Transducción de SeñalRESUMEN
A correlation between MUC1 expression in renal cell carcinomas (RCCs) and the clinical stages was previously demonstrated. To assess whether MUC1 expression is causally related to malignant tumor behavior, MUC1 cDNA was stably transfected into a renal carcinoma cell line SN12C that expresses trace levels of MUC1. MUC1 with sialylated carbohydrate chains was detected on the surface of transfected cells in two independent experiments. There was no correlation between MUC1 expression and in vitro growth and motility. In vivo growth of the transfectants at the site of orthotopic transplantation in nude mice was slower than mock transfected cells. Therefore, MUC1 alone did not seem to confer a malignant phenotype to RCCs.