Abstract
RNA granules and exosomes produced by tumour cells under various stresses in the microenvironment act as critical determinants of cell survival by promoting angiogenesis, cancer metastasis, chemoresistance, and immunosuppression. Meanwhile, developmental cancer/testis (CT) antigens that are normally sequestered in male germ cells of the testes, but which are overexpressed in malignant tumour cells, can function as tumour antigens triggering immune responses. As CT antigens are potential vaccine candidates for use in cancer immunotherapy, they could be targeted together with crosstalk between stress granules, exosomes, and immune cells for a synergistic effect. In this review, we describe the effects of exosomes and exosomal components presented to the recipient cells under different types of stresses on immune cells and cancer progression. Furthermore, we discuss their significance for cancer immunity, as well as the outlook for their future application.
Highlights
The tumour microenvironment consists of components, including cancer-associated fibroblasts (CAFs), immune-inflammatory cells, adipose cells, neuroendocrine cells, lymphatic vascular networks, and the extracellular matrix (ECM) [1]
As seen from the tumour–host crosstalk and cell-to-cell communication at the primary tumour site and distant sites, a multicentric adaptive therapeutic approach is needed for the efficient treatment of cancer [134]
The careful examination of signalling pathways presents an intertwining network involving the partial recruitment of immune cells at each stage, either to check cancer progression or sometimes to escape cancer progression
Summary
The tumour microenvironment consists of components, including cancer-associated fibroblasts (CAFs), immune-inflammatory cells, adipose cells, neuroendocrine cells, lymphatic vascular networks, and the extracellular matrix (ECM) [1]. After the initial stress in the cancer microenvironment is sensed by eukaryotic initiation factor (eIF)-2α kinases, such as general control nonderepressible-2, heme-regulated inhibitor, protein kinase R (PKR), and PKR-like endoplasmic reticulum kinase (PERK), SG formation is triggered [30] It aids in the adaptation and survival of tumour cells, which are exposed to the increased demand for oxygen and nutrients during solid tumour development [31]. As a result of phosphorylation of eIF-2 by stress, polysomes are disassembled and stalled messenger ribonucleoprotein particles arise in the cytoplasm [34] These consist of translation initiation factors, 40s ribosomal subunits, and 48S complexes, as well as a subset of RNA-binding proteins It is important in YB-1 functions under stress, and modulating proteolytic cleavage of YB-1 in the cancerous site could affect cell proliferation, invasion, and migration of immune cells
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