We are analyzing https://link.springer.com/article/10.1186/s12943-022-01652-3.

Title:
Targeting RNA N6-methyladenosine modification: a precise weapon in overcoming tumor immune escape | Molecular Cancer
Description:
Immunotherapy, especially immune checkpoint inhibitors (ICIs), has revolutionized the treatment of many types of cancer, particularly advanced-stage cancers. Nevertheless, although a subset of patients experiences dramatic and long-term disease regression in response to ICIs, most patients do not benefit from these treatments. Some may even experience cancer progression. Immune escape by tumor cells may be a key reason for this low response rate. N6-methyladenosine (m6A) is the most common type of RNA methylation and has been recognized as a critical regulator of tumors and the immune system. Therefore, m6A modification and related regulators are promising targets for improving the efficacy of tumor immunotherapy. However, the association between m6A modification and tumor immune escape (TIE) has not been comprehensively summarized. Therefore, this review summarizes the existing knowledge regarding m6A modifications involved in TIE and their potential mechanisms of action. Moreover, we provide an overview of currently available agents targeting m6A regulators that have been tested for their elevated effects on TIE. This review establishes the association between m6A modifications and TIE and provides new insights and strategies for maximizing the efficacy of immunotherapy by specifically targeting m6A modifications involved in TIE.
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Keywords {🔍}

pubmed, article, google, scholar, cas, cells, cancer, cell, central, rna, tumor, modification, promotes, mrna, tie, mettl, fto, expression, immune, wang, nmethyladenosine, zhang, ythdf, alkbh, methylation, binding, translation, liu, immunotherapy, res, stem, targeting, proteins, nat, protein, studies, regulates, mol, chen, signaling, promote, pathway, regulating, dcs, ythdc, growth, carcinoma, glycolysis, antigen, stability,

Topics {✒️}

circrna-sore/mir-103a-2-5p/mir-660-3p/wnt2b/β-catenin pathway aff4/nf-κb/myc signaling network wnt/β-catenin signalling pathway axin1/wnt/β-catenin signaling m6a individual-nucleotide-resolution cross-linking mettl3/mir-143-3p/vash1 pathway malat1/mir-26b/hmga2 axis activating wnt/β-catenin pathway quantitative single-base-resolution sequencing regulating tgfbr1/smad2/smad3 pathway n6-methyladenosine-dependent translational enhancement wnt/β-catenin pathway dependent e2f-transcription super-enhancer mettl3-mediated n6-methyladenosine modification alkbh5/neat1/cxcl8/il-8 pathway [108] β-catenin/abcc9 axis alpha-ketoglutarate-dependent dioxygenase family β-catenin signaling pathway α-ketoglutaric acid-dependent manner m6a-crosslinking-exonuclease-sequencing m6am antibody-independent technique mazter-seq modulate pl-l1/pd-1 expression single-nucleotide-resolution mapping mir-20a-5p anti-pd-1/pd-l1 antibodies main components mettl3/mettl14/wtap quantitative single-base-resolution article download pdf regulating β-catenin signaling circrna-sore mrna e2f-driven gene expression post-transcriptional super-enhancer hnrnpa2/b1 activates cyclooxygenase-2 transforming growth factor-β m6a-crosslinking-exonuclease-sequencing rna n6-methyladenosine methyltransferase rna n6-methyladenosine methyltransferase hypoxia-inducible factor-1α a-glut1-mtorc1 axis human hnrnp a2/b1 anti-tumour immunity controlled il7r/jak/stat5 pathway [100] anti-pd-l1 antibody n6-methyladenosine-dependent regulation overcoming immunotherapy-related challenges fluorescence anisotropy-based assay a-igf2bp2-dependent mechanism precursor mir-143-3p pi3k/akt signaling pathway constant t-cell selection

Questions {❓}

Cancer-generated lactic acid: a regulatory, immunosuppressive metabolite?

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         headline:Targeting RNA N6-methyladenosine modification: a precise weapon in overcoming tumor immune escape
         description:Immunotherapy, especially immune checkpoint inhibitors (ICIs), has revolutionized the treatment of many types of cancer, particularly advanced-stage cancers. Nevertheless, although a subset of patients experiences dramatic and long-term disease regression in response to ICIs, most patients do not benefit from these treatments. Some may even experience cancer progression. Immune escape by tumor cells may be a key reason for this low response rate. N6-methyladenosine (m6A) is the most common type of RNA methylation and has been recognized as a critical regulator of tumors and the immune system. Therefore, m6A modification and related regulators are promising targets for improving the efficacy of tumor immunotherapy. However, the association between m6A modification and tumor immune escape (TIE) has not been comprehensively summarized. Therefore, this review summarizes the existing knowledge regarding m6A modifications involved in TIE and their potential mechanisms of action. Moreover, we provide an overview of currently available agents targeting m6A regulators that have been tested for their elevated effects on TIE. This review establishes the association between m6A modifications and TIE and provides new insights and strategies for maximizing the efficacy of immunotherapy by specifically targeting m6A modifications involved in TIE.
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