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IL-1β in breast cancer bone metastasis

Published online by Cambridge University Press:  01 March 2022

Jiabao Zhou
Affiliation:
Department of Oncology and Metabolism, University of Sheffield, Beech Hill Road, SheffieldS10 2RX, UK
Claudia Tulotta
Affiliation:
Institute for Experimental Pathology (ExPat), Center for Molecular Biology of Inflammation (ZMBE), Westfälische Wilhelms-Universität (WWU), 48149Münster, Germany
Penelope D. Ottewell*
Affiliation:
Department of Oncology and Metabolism, University of Sheffield, Beech Hill Road, SheffieldS10 2RX, UK
*
Author for correspondence: Penelope D. Ottewell, E-mail: [email protected]

Abstract

Bone is the most common site for advanced breast cancer to metastasise. The proinflammatory cytokine, interleukin-1β (IL-1β) plays a complex and contradictory role in this process. Recent studies have demonstrated that breast cancer patients whose primary tumours express IL-1β are more likely to experience relapse in bone or other organs. Importantly, IL-1β affects different stages of the metastatic process including growth of the primary tumour, epithelial to mesenchymal transition (EMT), dissemination of tumour cells into the blood stream, tumour cell homing to the bone microenvironment and, once in bone, this cytokine participates in the interaction between cancer cells and bone cells, promoting metastatic outgrowth at this site. Interestingly, although inhibition of IL-1β signalling has been shown to have potent anti-metastatic effects, inhibition of the activity of this cytokine has contradictory effects on primary tumours, sometimes reducing but often promoting their growth. In this review, we focus on the complex roles of IL-1β on breast cancer bone metastasis: specifically, we discuss the distinct effects of IL-1β derived from tumour cells and/or microenvironment on inhibition/induction of primary breast tumour growth, induction of the metastatic process through the EMT, promotion of tumour cell dissemination into the bone metastatic niche and formation of overt metastases.

Type
Review
Copyright
Copyright © The Author(s), 2022. Published by Cambridge University Press

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