Inflammation-Driven Breast Tumor Cell Plasticity: Stemness/EMT, Therapy Resistance and Dormancy

Area of Science:

• Oncology
• Cancer Biology
• Immunology

Background:

• Cancer cellular heterogeneity presents a major therapeutic hurdle.
• Tumor cell plasticity, including stemness and epithelial-to-mesenchymal transition (EMT), drives heterogeneity, therapy resistance, and dormancy.
• The tumor microenvironment, particularly chronic inflammation, significantly influences cancer progression.

Purpose of the Study:

• To review the role of inflammatory elements in driving key processes of tumor cell plasticity.
• To highlight how inflammation-associated myeloid cells, cytokines, and chemokines promote tumor cell remodeling.
• To explore the potential clinical benefits of targeting inflammatory elements in cancer therapy.

Main Methods:

• Review of recent findings on inflammation and cancer cell plasticity.
• Focus on breast cancer as a model system.
• Analysis of the roles of macrophages, TNFα, IL-6, CXCL8, and CXCL1.

Main Results:

• Inflammation-associated myeloid cells, pro-inflammatory cytokines (TNFα, IL-6), and chemokines (CXCL8, CXCL1) critically promote tumor cell remodeling.
• These inflammatory components regulate stemness/EMT, therapy resistance, and dormancy.
• Inflammatory elements are a common factor across different plasticity aspects.

Conclusions:

• Inflammation is a key driver of cancer cell plasticity, impacting stemness, therapy resistance, and dormancy.
• Targeting inflammatory pathways presents a promising therapeutic strategy for cancer treatment.
• Further research into targeting inflammation could lead to critical clinical benefits for cancer patients.