The cancer cell secretome drives cooperative manipulation of the tumour microenvironment to accelerate tumourigenesis

Shona Ritchie; Daniel A Reed; Brooke A Pereira; Paul Timpson

doi:10.12703/r/10-4

The cancer cell secretome drives cooperative manipulation of the tumour microenvironment to accelerate tumourigenesis

Fac Rev. 2021 Jan 19:10:4. doi: 10.12703/r/10-4. eCollection 2021.

Authors

Shona Ritchie^{1

2}, Daniel A Reed^{1

2}, Brooke A Pereira^{1

2}, Paul Timpson^{1

2}

Affiliations

¹ The Kinghorn Cancer Centre, Garvan Institute of Medical Research, Sydney, New South Wales 2010, Australia.
² St. Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney, New South Wales 2010, Australia.

PMID: 33659922
PMCID: PMC7894270
DOI: 10.12703/r/10-4

Abstract

Cellular secretions are a fundamental aspect of cell-cell and cell-matrix interactions in vivo. In malignancy, cancer cells have an aberrant secretome compared to their non-malignant counterparts, termed the "cancer cell secretome". The cancer cell secretome can influence every stage of the tumourigenic cascade. At the primary site, cancer cells can secrete a multitude of factors that facilitate invasion into surrounding tissue, allowing interaction with the local tumour microenvironment (TME), driving tumour development and progression. In more advanced disease, the cancer cell secretome can be involved in extravasation and metastasis, including metastatic organotropism, pre-metastatic niche (PMN) preparation, and metastatic outgrowth. In this review, we will explore the latest advances in the field of cancer cell secretions, including its dynamic and complex role in activating the TME and potentiating invasion and metastasis, with comments on how these secretions may also promote therapy resistance.

Keywords: Cancer cell secretome; Pre-metastatic niche; Stroma; Tumour microenvironment.

Publication types

Review

Grants and funding

Shona Ritchie is supported by the University of New South Wales (UNSW) University International Postgraduate Award. Brooke. A Pereira is supported by a Sydney Catalyst Seed Funding Grant. Paul Timpson is supported by the Len Ainsworth Fellowship in Pancreatic Cancer Research and is a National Health and Medical Research Council (NHMRC) Senior Research Fellow. This work was made possible by an Avner Pancreatic Cancer Foundation Grant. This work was supported by Suttons, Sydney Catalyst, Australian Research Council (ARC), NHMRC, Cancer Council NSW, Cancer Institute NSW, National Breast Cancer Foundation (NBCF), and St. Vincent’s Clinic Foundation.