Cellular interactions in tumor microenvironment during breast cancer progression: new frontiers and implications for novel therapeutics

Front Immunol. 2024 Mar 12:15:1302587. doi: 10.3389/fimmu.2024.1302587. eCollection 2024.

Abstract

The breast cancer tumor microenvironment (TME) is dynamic, with various immune and non-immune cells interacting to regulate tumor progression and anti-tumor immunity. It is now evident that the cells within the TME significantly contribute to breast cancer progression and resistance to various conventional and newly developed anti-tumor therapies. Both immune and non-immune cells in the TME play critical roles in tumor onset, uncontrolled proliferation, metastasis, immune evasion, and resistance to anti-tumor therapies. Consequently, molecular and cellular components of breast TME have emerged as promising therapeutic targets for developing novel treatments. The breast TME primarily comprises cancer cells, stromal cells, vasculature, and infiltrating immune cells. Currently, numerous clinical trials targeting specific TME components of breast cancer are underway. However, the complexity of the TME and its impact on the evasion of anti-tumor immunity necessitate further research to develop novel and improved breast cancer therapies. The multifaceted nature of breast TME cells arises from their phenotypic and functional plasticity, which endows them with both pro and anti-tumor roles during tumor progression. In this review, we discuss current understanding and recent advances in the pro and anti-tumoral functions of TME cells and their implications for developing safe and effective therapies to control breast cancer progress.

Keywords: breast cancer; immune cells; metastasis; stroma; tumor microenvironment.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Communication
  • Humans
  • Immune Evasion
  • Neoplasms*
  • Stromal Cells
  • Tumor Microenvironment*

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. AA and PM were supported by a grant from the Breast Cancer Research Foundation of Alabama (project number: 0142-22P).