Failure of wild-type or a mutant form of protein kinase C-α to transform fibroblasts

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Abstract
A MUTANT form of the α-isoform of protein kinase C (PKC) was recently isolated from an ultraviolet radiation-induced murine fibrosarcoma cell line and reported to transform mouse BALB/c 3T3 fibroblasts on transfection1. Four point mutations in the regulatory domain were assumed to be responsible for its oncogenicity and unusual preference for membrane localization. Here, we report that overexpression of the reported mutant PKCα complementary DNA in three fibroblast cell lines, including BALB/c 3T3, does not enable these cells to grow in soft agar or nude mice. In addition, this mutant PKCα form seems to be indistinguishable from the wild-type PKCα with respect to its dependence on co-factors, phorbol ester binding, subcellular distribution and its effects on growth and morphology. These results fail to confirm the previous study1 and indicate that overexpression of either the wild-type or the reported mutant form of PKCα does not transform rodent fibroblasts.