Résumé
A point mutation in the protein kinase Cα (PKCα) gene has been discovered in a subpopulation of human pituitary tumors characterized by their invasive phenotype. Here we show that: (1) thyroid tumors can express the PKCα mutation detected in a subpopulation of follicular adenomas and carcinomas, and (2) mutated PKCα has modified enzymatic properties as compared to wild-type PKCα. It has lost its capacity to phosphorylate the S17R substrate and exhibits a higher sensitivity to degradation as compared to wild-type PKCα. In conclusion, the presence of the PKCα mutant in tumors other than pituitary tumors and the observation that the presence of the point mutation induces changes in PKCα properties suggest the involvement of this mutant in tumorigenesis.