The concept of epithelial–mesenchymal plasticity (EMP), which describes the dynamic flux within the spectrum of phenotypic states that invasive carcinoma cells may reside, is being increasingly recognised for its role in cancer progression and therapy resistance. The myriad of events that are able to induce EMP, as well as the more recently characterised control loops, results in dynamic transitions of cancerous epithelial cells to more mesenchymal-like phenotypes through an epithelial–mesenchymal transition (EMT), as well as the reverse transition from mesenchymal phenotypes to an epithelial one. The significance of EMP, in its ability to drive local invasion, generate cancer stem cells and facilitate metastasis by the dissemination of circulating tumour cells (CTCs), highlights its importance as a targetable programme to combat cancer morbidity and mortality. The focus of this review is to consolidate the existing knowledge on the strategies currently in development to combat cancer progression via inhibition of specific facets of EMP. The prevalence of relapse due to therapy resistance and metastatic propensity that EMP endows should be considered when designing therapy regimes, and such therapies should synergise with existing chemotherapeutics to benefit efficacy. To further improve upon EMP-targeted therapies, it is imperative to devise monitoring strategies to assess the impact of such treatments on EMP-related phenomenon such as CTC burden, chemosensitivity/-resistance and micrometastasis in patients.
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October 2017
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Cover Image
The 26S proteasome. Image kindly provided by Professor Joel Kowit from his work Degradation, a depiction in stained glass of the 26S proteasome (see http://joelkowit.com). In this issue of the Biochemical Journal, VerPlank and Goldberg describe how phosphorylation of the proteasome regulates protein breakdown by reviewing the ability of several kinases to alter proteasome function; see pages 3355–3371 for further details.
Review Article|
September 20 2017
Targeting epithelial–mesenchymal plasticity in cancer: clinical and preclinical advances in therapy and monitoring
Sugandha Bhatia;
Sugandha Bhatia
*
1Institute of Health and Biomedical Innovation and School of Biomedical Sciences, Queensland University of Technology, Brisbane, Australia
2Translational Research Institute, Brisbane, Australia
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James Monkman;
James Monkman
*
1Institute of Health and Biomedical Innovation and School of Biomedical Sciences, Queensland University of Technology, Brisbane, Australia
2Translational Research Institute, Brisbane, Australia
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Alan Kie Leong Toh;
Alan Kie Leong Toh
1Institute of Health and Biomedical Innovation and School of Biomedical Sciences, Queensland University of Technology, Brisbane, Australia
2Translational Research Institute, Brisbane, Australia
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Shivashankar H. Nagaraj;
Shivashankar H. Nagaraj
1Institute of Health and Biomedical Innovation and School of Biomedical Sciences, Queensland University of Technology, Brisbane, Australia
2Translational Research Institute, Brisbane, Australia
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Erik W. Thompson
1Institute of Health and Biomedical Innovation and School of Biomedical Sciences, Queensland University of Technology, Brisbane, Australia
2Translational Research Institute, Brisbane, Australia
Correspondence: Erik W. Thompson (e2.thompson@qut.edu.au)
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Publisher: Portland Press Ltd
Received:
May 15 2017
Revision Received:
August 01 2017
Accepted:
August 07 2017
Online ISSN: 1470-8728
Print ISSN: 0264-6021
© 2017 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society
2017
Biochem J (2017) 474 (19): 3269–3306.
Article history
Received:
May 15 2017
Revision Received:
August 01 2017
Accepted:
August 07 2017
Citation
Sugandha Bhatia, James Monkman, Alan Kie Leong Toh, Shivashankar H. Nagaraj, Erik W. Thompson; Targeting epithelial–mesenchymal plasticity in cancer: clinical and preclinical advances in therapy and monitoring. Biochem J 1 October 2017; 474 (19): 3269–3306. doi: https://doi.org/10.1042/BCJ20160782
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