The important role of PKC in controlling polyploidy formation in cultured fibrosarcoma cell line.

Induction of polyploidization by colcemid in cultured fibrosarcoma cells (Meth-A cells) was examined. Activators of protein kinase C (PKC), phorbol 12-myristate 13-acetate (PMA) and ATP, inhibited colcemid-induced polyploidization, but not colcemid-induced cell proliferation cessation. These findings suggest that a down-regulation of PKC activity results in checkpoint "dysfunction" which induces polyploidization and that inhibition of polyploidization induction by PMA and ATP is not a result of the inhibition of colcemid-induced depolymerization of tubulin.