Influence of Immune Myeloid Cells on the Extracellular Matrix During Cancer Metastasis

David Jiang, Su Yin Lim*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

26 Citations (Scopus)
14 Downloads (Pure)


The extracellular matrix (ECM) is one of the most important components within the tumor microenvironment that supports cancer development and metastasis. Under normal physiological conditions, the ECM is a tightly regulated network providing structural and biochemical support. However, the ECM becomes highly disorganized during neoplastic progression and consequently, stimulates cancer cell transformation, growth and spread. Cancer development and progression is also known to greatly benefit from the support of immune myeloid cells, which have multiple pro-tumorigenic functions including promoting tumor growth, migration and invasion, stimulating angiogenesis and suppressing anti-tumor responses. An increasing number of studies have shown that myeloid cells alter the ECM to support metastatic cancer progression and in turn, the ECM can influence the function of infiltrating myeloid cells. However, the exact nature of this relationship, such as the mechanisms employed and their molecular targets remains unclear. This review discusses evidence for the reciprocal dependence of myeloid cells and the tumor ECM for efficient tumor development and explores potential mechanisms involved in these interactions. A better understanding of this relationship has exciting implications for the development of new therapeutic treatments for metastatic cancer.

Original languageEnglish
Pages (from-to)45-61
Number of pages17
JournalCancer Microenvironment
Issue number1
Publication statusPublished - 1 Apr 2016
Externally publishedYes

Bibliographical note

Copyright the Author(s) 2016. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.


  • Cancer metastasis
  • Cancer therapy
  • Immune cells
  • Metalloproteinases
  • Myeloid cells
  • Tumor microenvironment


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