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Abstract
Cross talk between cancer cells and the immune system is determinant for cancer progression. Emerging evidence demonstrates that GC characteristics such as metastasis, treatment resistance, and disease recurrence are associated with a tumor subpopulation called gastric cancer stem cells (GCSCs). However, the specific interaction between GCSCs and the immune microenvironment is still under investigation. Although immune evasion has been well described for cancer stem cells (CSCs), recent studies show that GCSCs can also regulate the immune system and even benefit from it. This review will provide an overview of bidirectional interactions between CSCs and immune cells in GC, compiling relevant data about how CSCs can induce leukocyte reprogramming, resulting in pro-tumoral immune cells that orchestrate promotion of metastasis, chemoresistance, tumorigenicity, and even increase in number of cancer cells with stem properties. Some immune cells studied are tumor-associated macrophages (TAMs), neutrophils, Th17 and T regulatory (Treg) cells, mesenchymal stem cells (MSCs), and cancer-associated fibroblasts (CAFs), as well as the signaling pathways involved in these pro-tumoral activities. Conversely, although there are cytotoxic leukocytes that can potentially eliminate GCSCs, we describe mechanisms for immune evasion in GCSCs and their clinical implications. Furthermore, we describe current available immunotherapy targeting GCSC-related markers as possible treatment for GC, discussing how the CSC-modified immune microenvironment can mitigate or inactivate these immunotherapies, limiting their effectiveness. Finally, we summarize key concepts and relevant evidence to understand the cross talk between GCSCs and the immune microenvironment as an important process for effective design of therapies against GCSCs that improve the outcome of patients with GC.
Highlights
Non-communicable diseases cancer stand out as the main cause of death in the world [1]
One of the most studied mechanisms that show how H. pylori promotes gastric cancer stem cells (GCSCs) is through its cytotoxin-associated gene A (CagA) protein, which in co-culture experiments has been demonstrated to be responsible for the increase of gastric cells with epithelial–mesenchymal transition (EMT) and cancer stem cells (CSCs) properties, like CD44 expression, in a mechanism mediated by E-cadherin, NF-kB, and Zeb1/2 transcription factors [33]
The influence that CSCs exert over leukocytes is dependent of the specific CSC phenotype, due to the different expression of cytokines and other factors, such as RNA contained in exosomes and immunological checkpoints
Summary
Non-communicable diseases cancer stand out as the main cause of death in the world [1]. One of the most studied mechanisms that show how H. pylori promotes GCSC is through its cytotoxin-associated gene A (CagA) protein, which in co-culture experiments has been demonstrated to be responsible for the increase of gastric cells with EMT and CSC properties, like CD44 expression, in a mechanism mediated by E-cadherin, NF-kB, and Zeb1/2 transcription factors [33].
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