Abstract
Colorectal cancer (CRC) has the second highest mortality rate among all cancers worldwide. Surgery, chemotherapy, radiotherapy, molecular targeting and other treatment methods have significantly prolonged the survival of patients with CRC. Recently, the emergence of tumor immunotherapy represented by immune checkpoint inhibitors (ICIs) has brought new immunotherapy options for the treatment of advanced CRC. As the efficacy of ICIs is closely related to the tumor immune microenvironment (TME), it is necessary to clarify the relationship between the immune microenvironment of CRC and the efficacy of immunotherapy to ensure that the appropriate drugs are selected. We herein review the latest research progress in the immune microenvironment and strategies related to immunotherapy for CRC. We hope that this review helps in the selection of appropriate treatment strategies for CRC patients.
Highlights
Colorectal cancer (CRC) is a common malignant tumor of the digestive system
Natural killer (NK) cells bind to NKG2D interaction ligands through antibodydependent cell-mediated cytotoxicity (ADCC) or receptors, degranulate and release cytotoxic perforin and granzyme, induce signal transduction, and kill virus-infected cells and tumor cells [114]
Hu et al found that cancer associated fibroblasts (CAF) secrete exosomes, resulting in a significant increase in the level of miR-92a-3p in CRC cells, activating the Wnt/b- catenin pathway and inhibiting mitochondrial apoptosis by directly inhibiting FBXW7 and MOAP1; the effect is to promote stemness, epithelial-mesenchymal transition (EMT), metastasis and 5-FU/L-OHP resistance in CRC [50]
Summary
Colorectal cancer (CRC) is a common malignant tumor of the digestive system. Worldwide, CRC ranks third in the incidence rate and second in the mortality rate among malignant tumors [1]. NK cells bind to NKG2D interaction ligands through antibodydependent cell-mediated cytotoxicity (ADCC) or receptors, degranulate and release cytotoxic perforin and granzyme, induce signal transduction, and kill virus-infected cells and tumor cells [114] Compared with those in adjacent normal tissues, NK cell levels in CRC tissues are low, suggesting that less NK cell infiltration may be one of the mechanisms of TME immune escape [115]. Hu et al found that CAFs secrete exosomes, resulting in a significant increase in the level of miR-92a-3p in CRC cells, activating the Wnt/b- catenin pathway and inhibiting mitochondrial apoptosis by directly inhibiting FBXW7 and MOAP1; the effect is to promote stemness, EMT, metastasis and 5-FU/L-OHP resistance in CRC [50]. Panitumumab, the first fully humanized IgG2 monoclonal antibody, displays a high affinity for EGFR, and its mechanism of TABLE 1 | Summary of antiangiogenic therapy for colorectal cancer (CRC)
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