A tale of three PKCs: epsilon emerges as a driver of pre-neoplastic phenotypes.

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This article has been peer reviewed. It was published in: Cell Cycle.

Volume 10, Issue 3, February 2011, Pages 379.

The published version is available at DOI: 10.4161/cc.10.3.14740. Copyright © Landes BioScience.


The concept that classical and novel PKCs exert divergent outcomes in cancer has been long appreciated (reviewed in ref. 1). The PKC family of serine-threonine kinases is comprised of ten related members, including “classical” (cPCKs α, β, and γ), “atypical” (aPKCs ι/λ and ζ), and “novel” (nPKC δ, ε, η, and µ) subclasses according to structural motifs, calcium requirement and mechanisms of activation. The individual PKCs regulate diverse and sometimes opposing cellular processes such as proliferation, apoptosis, migration/motility, differentiation and, most notably, are thought to play unique roles in cancer development and progression. The potential impact of PKCs on tumor development was realized almost three decades ago when PKCs were identified as intracellular receptors for tumor-inducing phorbol esters.2 These initial discoveries ignited a season of discovery for discerning the overall influence of PKCs in tumorigenesis and tumor progression (reviewed in ref. 3).

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