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Cited by 221MicroRNA in disease regulationCancer Immunotherapy and BiomarkersImmune cells in cancer

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The role of cancer-derived microRNAs in cancer immune escape

Open access
Yi, Ming, Xu, Linping, Jiao, Ying, Luo, Suxia, Li, Anping, Wu, Kongming·2020·Journal of Hematology & Oncology
DOI 10.1186/s13045-020-00848-8PMC PMC7103070
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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.

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Fig. 1 The mechanisms by which cancer cells escape from immune attack of immune effector cells. Firstly, 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. Secondly, overexpressed immune checkpoints or their ligands such as PD-L1 on cancer cells promote the formation of exhausted TILs. Thirdly, cancer cells tend to harbor alterations in antigen processing machinery, which result in the loss of tumor-associated antigens and neoantigens. Mutations in major histocompatibility complex class I (MHC-I), proteasome subunits latent membrane protein, as well as transporter associated with antigen processing reduce the presentation of recognizable targets on cancer cells. Fourthly, overexpressed HLA-G on cancer cells binds to the inhibitory receptors on effector cells such as CTLs and NKs, leading to the suppression of the cytotoxic activities of these effector cells. Lastly, cancer cells could escape immune attack by downregulating NKG2D ligands including MICA, MICB, and UL16-binding protein. TAP transporter associated with antigen processing, MHC-I major histocompatibility complex class I, MICA/B MHC-I chain-related molecules A/B, IDO indoleamine 2, 3-dioxygenase, ULBP UL16-binding protein
Fig. 1 The mechanisms by which cancer cells escape from immune attack of immune effector cells. Firstly, 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. Secondly, overexpressed immune checkpoints or their ligands such as PD-L1 on cancer cells promote the formation of exhausted TILs. Thirdly, cancer cells tend to harbor alterations in antigen processing machinery, which result in the loss of tumor-associated antigens and neoantigens. Mutations in major histocompatibility complex class I (MHC-I), proteasome subunits latent membrane protein, as well as transporter associated with antigen processing reduce the presentation of recognizable targets on cancer cells. Fourthly, overexpressed HLA-G on cancer cells binds to the inhibitory receptors on effector cells such as CTLs and NKs, leading to the suppression of the cytotoxic activities of these effector cells. Lastly, cancer cells could escape immune attack by downregulating NKG2D ligands including MICA, MICB, and UL16-binding protein. TAP transporter associated with antigen processing, MHC-I major histocompatibility complex class I, MICA/B MHC-I chain-related molecules A/B, IDO indoleamine 2, 3-dioxygenase, ULBP UL16-binding proteinCC BY · PubMed Central
Fig. 2 Cancer-derived miRNAs regulate immune evasion via modulating the expression profiles within cancer cells. Firstly, some immune modulatory miRNAs disturb antigen processing and presentation by targeting one or multiple components of APM (e.g., TAP1, LMP8, LMP9, and LMP10) and MHC-I molecules in cancer cells. Secondly, the loss of some HLA-G-targeting miRNAs is highly related with increased HLA-G expression, which is a well-accepted immune tolerant moelcule. Thirdly, cancer cells could escape immune attack by downregulating NKG2D ligands (MICA/B and ULBP2) in post-transcriptional level. Increased MICA/B- or ULBP2-targeting miRNAs protect cancer cells from immune clearence of NKs and CTLs. Fourthly, altered miRNA expressio pattern upregulates PD-L1 level in cancer cells. Lastly, dysregulated miRNA profiles change the metabolism of cancer cells. Increased IDO1 further hampered the normal immune survelliance. The miRNAs promoting anti-cancer immune response are exihibited in boxes with green background while the miRNAs inhbiting anti-cancer immune reponse are showed in boxes with red background. Upregualted immunostiumlatory miRNAs together with downregualted immunosuppressive miRNAs contribute to cancer immune evasion. APM antigen processing machinery, TAP transporter associated with antigen processing, MHC-I major histocompatibility complex class I, LMP proteasome subunits latent membrane protein, MICA/B MHC-I chain-related molecules A/B, ULBP UL16-binding protein, CTL cytotoxic T lymphocyte, IDO indoleamine 2, 3-dioxygenase
Fig. 2 Cancer-derived miRNAs regulate immune evasion via modulating the expression profiles within cancer cells. Firstly, some immune modulatory miRNAs disturb antigen processing and presentation by targeting one or multiple components of APM (e.g., TAP1, LMP8, LMP9, and LMP10) and MHC-I molecules in cancer cells. Secondly, the loss of some HLA-G-targeting miRNAs is highly related with increased HLA-G expression, which is a well-accepted immune tolerant moelcule. Thirdly, cancer cells could escape immune attack by downregulating NKG2D ligands (MICA/B and ULBP2) in post-transcriptional level. Increased MICA/B- or ULBP2-targeting miRNAs protect cancer cells from immune clearence of NKs and CTLs. Fourthly, altered miRNA expressio pattern upregulates PD-L1 level in cancer cells. Lastly, dysregulated miRNA profiles change the metabolism of cancer cells. Increased IDO1 further hampered the normal immune survelliance. The miRNAs promoting anti-cancer immune response are exihibited in boxes with green background while the miRNAs inhbiting anti-cancer immune reponse are showed in boxes with red background. Upregualted immunostiumlatory miRNAs together with downregualted immunosuppressive miRNAs contribute to cancer immune evasion. APM antigen processing machinery, TAP transporter associated with antigen processing, MHC-I major histocompatibility complex class I, LMP proteasome subunits latent membrane protein, MICA/B MHC-I chain-related molecules A/B, ULBP UL16-binding protein, CTL cytotoxic T lymphocyte, IDO indoleamine 2, 3-dioxygenaseCC BY · PubMed Central
Fig. 3 Cancer cells-derived miRNAs regulating immune evasion via exosomes or vehicles. Cancer-derived miRNAs could be packed into exosomes or microvesicles, which are transferred to numerous TILs and shape an immunosuppressive microenvironment. Cancer-derived exosomal miRNAs impair the cytotoxicity of effector cells, inducing the polarization of macrophages toward M2-like phenotype, promoting the expansion and the immunosuppressive activity of MDSCs, as well as inhibiting infiltration of lymphocytes via CAF-mediated matrix remodeling. TIL tumor-infiltrating lymphocyte, MDSC myeloid-derived suppressor cell, CAF cancer-associated fibroblast, TAM tumor-associated macrophage
Fig. 3 Cancer cells-derived miRNAs regulating immune evasion via exosomes or vehicles. Cancer-derived miRNAs could be packed into exosomes or microvesicles, which are transferred to numerous TILs and shape an immunosuppressive microenvironment. Cancer-derived exosomal miRNAs impair the cytotoxicity of effector cells, inducing the polarization of macrophages toward M2-like phenotype, promoting the expansion and the immunosuppressive activity of MDSCs, as well as inhibiting infiltration of lymphocytes via CAF-mediated matrix remodeling. TIL tumor-infiltrating lymphocyte, MDSC myeloid-derived suppressor cell, CAF cancer-associated fibroblast, TAM tumor-associated macrophageCC BY · PubMed Central

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Metadata

Authors
Yi, M., Xu, L., Jiao, Y., Luo, S., Li, A., & Wu, K.
Affiliations
  • Tongji Hospital (CN)
  • Zhengzhou University (CN)
Corresponding author
Wu, Kongming
ORCID
Venue
Journal of Hematology & Oncology
Publisher
Springer Science and Business Media LLC
Published
2020-03-28
Volume
13
Issue
1
Pages
25-25
ISSN
1756-8722 (ISSN-L)
DOI
10.1186/s13045-020-00848-8
PMC
PMC7103070
OpenAlex
W3013629088
Cited by
221
References
153
Citations by year
2026: 6 · 2025: 33 · 2024: 24 · 2023: 47 · 2022: 44 · 2021: 47 · 2020: 18
FWCI
4.00
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Hematology & Oncology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Natural Science Foundation of China (81874120, 81572608)
  • Wuhan Science and Technology Bureau (2017060201010170)
  • Henan science and technology open cooperation project (162106000021)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
  • Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
Keywords
tumor immune evasion, tumor microenvironment, immune checkpoint pathways, MHC downregulation, interferon pathway, exosomes, microvesicles, tumor immunogenicity, post-transcriptional regulation, antitumor immunity, therapeutic target
MeSH terms
Animals, Antigens, Neoplasm, Humans, Immunotherapy, Neoplasms, Tumor Escape, MicroRNAs, Tumor Microenvironment

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