Abstract
During malignant transformation, accumulated somatic mutations endow cancer cells with increased invasiveness and immunogenicity. Under selective pressure, these highly immunogenic cancer cells develop multiple strategies to evade immune attack. It has been well established that cancer cells could downregulate the expression of major histocompatibility complex, acquire alterations in interferon pathway, and upregulate the activities of immune checkpoint pathways. Besides, cancer cells secret numerous cytokines, exosomes, and microvesicles to regulate the functions and abundances of components in the tumor microenvironment including immune effector cells and professional antigen presentation cells. As the vital determinant of post-transcriptional regulation, microRNAs (miRNAs) not only participate in cancer initiation and progression but also regulate anti-cancer immune response. For instance, some miRNAs affect cancer immune surveillance and immune escape by interfering the expression of immune attack-associated molecules. A growing body of evidence indicated that cancer-derived immune modulatory miRNAs might be promising targets to counteract cancer immune escape. In this review, we summarized the role of some miRNAs in cancer immune escape and discussed their potential clinical application as treatment targets.
Highlights
Robust anti-cancer immune response consists of a series of stepwise immune events including the release of cancer-associated antigens, the processing and presentation of antigen presentation cells (APCs), the priming and activation of naïve T cells, the trafficking and migration of activated T cells, and the tumor-killing activity of effector cells [1, 2]
Overexpressed Human leukocyte antigen (HLA)-G on cancer cells binds to the inhibitory receptors on effector cells such as Cytotoxic T lymphocyte (CTL) and NKs, leading to the suppression of the cytotoxic activities of these effector cells [62]
The major histocompatibility complex class I (MHC-I) chain-related molecules A/B and miRNAs The oncogenically transformed cells are susceptible to expressing a series of stress-induced ligands including MICA, MICB, and UL16-binding protein (ULBP) [70– 72]
Summary
Robust anti-cancer immune response consists of a series of stepwise immune events including the release of cancer-associated antigens, the processing and presentation of antigen presentation cells (APCs), the priming and activation of naïve T cells, the trafficking and migration of activated T cells, and the tumor-killing activity of effector cells [1, 2]. More and more studies demonstrated that cancer-derived microRNAs (miRNAs) are closely implicated in the formation of the immunosuppressive tumor microenvironment, disabled effector cells, as well as downregulated cancer immunogenicity [13, 14]. Other approaches could be utilized by cancer cells to produce immune evasion, such as inducing regulatory immune cells, acquiring disable antigen presentation machinery, upregulating immune checkpoints, and generating immunosuppressive microenvironment (Fig. 1) [27]. Immune inhibitory cytokines and immune checkpoints Tumor-derived cytokines especially TGF-β remarkably reshape the tumor immune microenvironment This immunosuppressive cytokine repertoire inhibits the functions of multiple effector cells, induces the differentiation of regulatory cells, and impedes the infiltration of T cells [43, 44]. Cancer cell-derived im-miRNAs target themselves and broadly regulate various immune components including MDSCs, Tregs, DCs, Tumor Recognization of cancer cell
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