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Front. Cell Dev. Biol. | doi: 10.3389/fcell.2018.00162

Oncogenic functions of MASTL kinase

  • 1Anzac Research Institute, Australia
  • 2Sydney Medical School, University of Sydney, Australia

MASTL kinase is a master regulator of mitosis, essential for ensuring that mitotic substrate phosphorylation is correctly maintained. It achieves this through the phosphorylation of alpha-endosulfine and subsequent inhibition of the tumour suppressor PP2A-B55 phosphatase. In recent years MASTL has also emerged as a novel oncogenic kinase that is upregulated in a number of cancer types, correlating with chromosome instability and poor patient survival. While the chromosome instability is likely directly linked to MASTL’s control of mitotic phosphorylation, several new studies indicated that MASTL has additional effects outside of mitosis and beyond regulation of PP2A-B55. These include control of normal DNA replication timing, and regulation of AKT/mTOR and Wnt/β-catenin oncogenic kinase signalling. In this review, we will examine the phenotypes and mechanisms for how MASTL, ENSA and PP2A-B55 deregulation drives tumour progression and metastasis. Finally, we will explore the rationale for the future development of MASTL inhibitors as new cancer therapeutics.

Keywords: cancer biology, Chromosome instability (CIN), AKT pathway, Mitosis, oncogene, MASTL

Received: 21 Sep 2018; Accepted: 08 Nov 2018.

Edited by:

Marcos Malumbres, Centro Nacional de Investigaciones Oncológicas CNIO - Fundación Cáncer FUCA, Spain

Reviewed by:

Philipp Kaldis, Agency for Science, Technology and Research (A*STAR), Singapore
Monica Alvarez, Centro Nacional de Investigaciones Oncológicas CNIO - Fundación Cáncer FUCA, Spain
Helfrid Hochegger, University of Sussex, United Kingdom  

Copyright: © 2018 Marzec and Burgess. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Andrew Burgess, Anzac Research Institute, Concord, Australia, andrew.burgess@anzac.edu.au