4.7 Review

Cancer Stem Cell Relationship with Pro-Tumoral Inflammatory Microenvironment

Journal

BIOMEDICINES
Volume 11, Issue 1, Pages -

Publisher

MDPI
DOI: 10.3390/biomedicines11010189

Keywords

cancer stem cells; inflammation; tumor microenvironment; leukocyte reprogramming; tumor-associated macrophages; cancer-associated fibroblasts; regulatory T cells

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Inflammatory processes and cancer stem cells (CSCs) play important roles in tumorigenesis. CSCs are associated with cancer properties such as metastasis, treatment resistance, and disease recurrence. This review explores the reciprocal interplay between CSCs and immune cells in the tumor microenvironment, highlighting how CSCs influence leukocyte reprogramming and promote pro-tumor immune cells. The study also emphasizes the potential of immune cells in eliminating CSCs, while addressing the immune evasion mechanisms in CSCs and their clinical implications.
Inflammatory processes and cancer stem cells (CSCs) are increasingly recognized as factors in the development of tumors. Emerging evidence indicates that CSCs are associated with cancer properties such as metastasis, treatment resistance, and disease recurrence. However, the precise interaction between CSCs and the immune microenvironment remains unexplored. Although evasion of the immune system by CSCs has been extensively studied, new research demonstrates that CSCs can also control and even profit from the immune response. This review provides an overview of the reciprocal interplay between CSCs and tumor-infiltrating immune cells, collecting pertinent data about how CSCs stimulate leukocyte reprogramming, resulting in pro-tumor immune cells that promote metastasis, chemoresistance, tumorigenicity, and even a rise in the number of CSCs. Tumor-associated macrophages, neutrophils, Th17 and regulatory T cells, mesenchymal stem cells, and cancer-associated fibroblasts, as well as the signaling pathways involved in these pro-tumor activities, are among the immune cells studied. Although cytotoxic leukocytes have the potential to eliminate CSCs, immune evasion mechanisms in CSCs and their clinical implications are also known. We intended to compile experimental findings that provide direct evidence of interactions between CSCs and the immune system and CSCs and the inflammatory milieu. In addition, we aimed to summarize key concepts in order to comprehend the cross-talk between CSCs and the tumor microenvironment as a crucial process for the effective design of anti-CSC therapies.

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