Targeting Oncoimmune Drivers of Cancer Metastasis

Chie Kudo-Saito1, Yukinori Ozaki1, Hiroshi Imazeki1

  • 1Department of Immune Medicine, National Cancer Center Research Institute, Tokyo 104-0045, Japan.

Cancers
|February 4, 2021
PubMed

Insights

Understanding cancer metastasis, including epithelial-mesenchymal transition (EMT) and cancer stem cells (CSCs), is crucial. This overview links tumor biology and immunity to improve treatments for residual cancer metastasis.

Area of Science:

  • Oncology
  • Immunology
  • Cell Biology

Background:

  • Residual metastasis remains a primary cause of cancer mortality.
  • Epithelial-mesenchymal transition (EMT) and cancer stem cells (CSCs) offer insights into metastasis but lack clinical translation.
  • Tumor cell evolution, driven by host environment interactions, creates complexity and hinders effective cancer management.

Purpose of the Study:

  • To provide an overview of the molecular and cellular links between tumor properties and host immunity.
  • To focus on the roles of EMT and CSCs in cancer metastasis.
  • To highlight therapeutic strategies targeting oncoimmune determinants for improved clinical application.

Main Methods:

  • Review of current literature on cancer metastasis, EMT, CSCs, and tumor-immune interactions.
  • Analysis of molecular and cellular mechanisms underlying tumor progression and immune evasion.
  • Identification of therapeutic targets within the tumor-immune microenvironment.

Main Results:

  • EMT and CSCs are key drivers of cancer metastasis, contributing to tumor heterogeneity and immune evasion.
  • Complex interactions between tumor cells and the host environment, including immune cells, promote metastasis.
  • Targeting oncoimmune factors presents a promising strategy to overcome treatment resistance.

Conclusions:

  • A comprehensive understanding of the interplay between tumor biology and immunity is essential for combating metastasis.
  • Therapeutic strategies should address both tumor-intrinsic properties (EMT, CSCs) and the tumor-immune microenvironment.
  • Developing practical clinical applications requires targeting key oncoimmune determinants to disrupt the metastatic cascade.

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