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Myeloid-derived suppressor cells: Key immunosuppressive regulators and therapeutic targets in colorectal cancer (Review)
Myeloid-derived suppressor cells: Key immunosuppressive regulators and therapeutic targets in colorectal cancer (Review)
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Myeloid-derived suppressor cells: Key immunosuppressive regulators and therapeutic targets in colorectal cancer (Review)
Myeloid-derived suppressor cells: Key immunosuppressive regulators and therapeutic targets in colorectal cancer (Review)

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Myeloid-derived suppressor cells: Key immunosuppressive regulators and therapeutic targets in colorectal cancer (Review)
Myeloid-derived suppressor cells: Key immunosuppressive regulators and therapeutic targets in colorectal cancer (Review)
Journal Article

Myeloid-derived suppressor cells: Key immunosuppressive regulators and therapeutic targets in colorectal cancer (Review)

2024
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Overview
Globally, colorectal cancer (CRC) is the third most common type of cancer. CRC has no apparent symptoms in the early stages of disease, and most patients receive a confirmed diagnosis in the middle or late disease stages. The incidence of CRC continues to increase, and the affected population tends to be younger. Therefore, determining how to achieve an early CRC diagnosis and treatment has become a top priority for prolonging patient survival. Myeloid-derived suppressor cells (MDSCs) are a group of bone marrow-derived immuno-negative regulatory cells that are divided into two subpopulations, polymorphonuclear-MDSCs and monocytic-MDSCs, based on their phenotypic similarities to neutrophils and monocytes, respectively. These cells can inhibit the immune response and promote cancer cell metastasis in the tumour microenvironment (TME). A large aggregation of MDSCs in the TME is often a marker of cancer and a poor prognosis in inflammatory diseases of the intestine (such as colonic adenoma and ulcerative colitis). In the present review, the phenotypic classification of MDSCs in the CRC microenvironment are first discussed. Then, the amplification, role and metastatic mechanism of MDSCs in the CRC TME are described, focusing on genes, gene modifications, proteins and the intestinal micro-environment. Finally, the progress in CRC-targeted therapies that aim to modulate the quantity, function and structure of MDSCs are summarized in the hope of identifying potential screening markers for CRC and improving CRC prognosis and therapeutic options.