The cellular and molecular components involved in pre-metastatic niche formation in colorectal cancer liver metastasis

Expert Rev Gastroenterol Hepatol. 2021 Apr;15(4):389-399. doi: 10.1080/17474124.2021.1848543. Epub 2020 Nov 30.

Abstract

Introduction: Liver metastasis is the main cause of death in colorectal cancer (CRC). Premetastatic niche (PMN), a favorable microenvironment for cancer cells colonization at the distant organ, plays a pivotal role in CRC liver metastasis (CRCLM). Our understanding of the mechanisms mediating the formation of liver PMN in CRC has been significantly advanced in recent years, there are still many challenges and questions that remain.Areas covered: This review covers cellular and molecular components, and the interaction of theprimary cancer with the resident microenvironment of the distant organ that leads to PMN formation in CRCLM based on the latest literature.Expert Opinion: Various cellular and molecular events are involved in the liver PMN formation in CRC such as bone marrow-derived cells (BMDCs), hepatic stellate cells, Kupffer cells, extracellular matrix, and CRC-derived factors. The formation of the liver PMN depends on a complex interaction of CRC with the liver microenvironment including BMDCs recruitment, vascularization, immunosuppression, inflammatory response, and extracellular matrix remodeling. This review firstly discusses on the cellular and molecular components contributing to the formation of the liver PMN in CRC, so as to provide new ideas for designing effective therapeutic strategies and prognostic markers for CRCLM.

Keywords: Colorectal cancer; cellular and molecular components; liver metastasis; pre-metastatic niche.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Communication
  • Colorectal Neoplasms / immunology
  • Colorectal Neoplasms / metabolism
  • Colorectal Neoplasms / pathology*
  • Cytokines / metabolism
  • Extracellular Matrix / metabolism
  • Extracellular Matrix / pathology
  • Humans
  • Liver Neoplasms / immunology
  • Liver Neoplasms / metabolism
  • Liver Neoplasms / secondary*
  • Signal Transduction
  • Tumor Microenvironment* / immunology

Substances

  • Cytokines