Abstract

The regulatory networks of cell polarization and polarity effector proteins have been subjects of feverish interest in the field of cell and developmental biology but many advances in the polarity research may have flown unnoticed past the radar of mainstream cancer biologist. However, recent findings suggesting important cell cycle gatekeeping functions for polarity proteins may change that. For example, PAR6 proteins interact with classical cancer driver signaling pathways, including MAPK and PI3K and moreover, PAR6 (PARD6) genes are frequently altered in various cancers. Mammalian genomes harbor three different PARD6 genes. Recent studies in breast cancer have suggested that different PARD6 genes are not only important players but may play even opposite roles during tumorigenesis.

Highlights

  • The regulatory networks of cell polarization and polarity effector proteins have been subjects of feverish interest in the field of cell and developmental biology but many advances in the polarity research may have flown unnoticed past the radar of mainstream cancer biologist

  • A current view is that PAR6 is a multimodular scaffold protein, which together with PAR3 forms a loose or non-constitutive complex with atypical protein kinase C and CDC42

  • PARD6B locus resides in a chromosomal region that is frequently amplified and overexpressed in breast cancer [4]

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Summary

Introduction

The regulatory networks of cell polarization and polarity effector proteins have been subjects of feverish interest in the field of cell and developmental biology but many advances in the polarity research may have flown unnoticed past the radar of mainstream cancer biologist. Par-6 is one of the partitioning-defective (par) genes identified by Kemphues et al in a landmark genetic screen, which discovered genes important for the first, asymmetric embryonic cell division in C.elegans [1]. This PAR3-PAR6-aPKC/ CDC42 or ‘PAR complex’ has a principal role in most if not all process where cellular asymmetry is important, for example asymmetric cell division, apico-basal and anterioposterior polarity, axon specification and directional migration [2, 3].

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