bims-rimeca Biomed News
on RNA methylation in cancer
Issue of 2022–06–19
twelve papers selected by
Sk Ramiz Islam, Saha Institute of Nuclear Physics
  1. The Potential Value of m6A RNA Methylation in the Development of Cancers Focus on Malignant Glioma.
  2. Detecting and Mapping N6-Methyladenosine on RNA/DNA Hybrids.
  3. METTL3-Mediated N6-Methyladenosine Modification of Trim59 mRNA Protects Against Sepsis-Induced Acute Respiratory Distress Syndrome.
  4. Mettl14-mediated m6A modification is essential for visual function and retinal photoreceptor survival.
  5. METTL3 inhibits anti-tumor immunity by targeting m6A-BHLHE41-CXCL1/CXCR2 axis to promote colorectal cancer.
  6. Characterization of m6A Methylation Modification Patterns in Colorectal Cancer Determines Prognosis and Tumor Microenvironment Infiltration.
  7. YTHDF3 Facilitates eIF2AK2 and eIF3A Recruitment on mRNAs to Regulate Translational Processes in Oxaliplatin-Resistant Colorectal Cancer.
  8. YTHDF2 promotes intrahepatic cholangiocarcinoma progression and desensitises cisplatin treatment by increasing CDKN1B mRNA degradation.
  9. AlkB RNA demethylase homologues and N6 -methyladenosine are involved in Potyvirus infection.
  10. METTL1 is required for non-homologous end joining repair and renders hepatocellular carcinoma resistant to radiotherapy.
  11. Comprehensive Analysis of the Function, Immune Profiles, and Clinical Implication of m1A Regulators in Lung Adenocarcinoma.
  12. An m6A/m5C/m1A/m7G-Related Long Non-coding RNA Signature to Predict Prognosis and Immune Features of Glioma.
  1. Front Immunol. 2022 ;13 917153
    The Potential Value of m6A RNA Methylation in the Development of Cancers Focus on Malignant Glioma.
    Fan Chen, Xuan Xie, Min Chao, Haiyan Cao, Liang Wang.
      N6-methyladenosine (m6A) RNA methylation is an epigenetic modification that has emerged in the last few years and has received increasing attention as the most abundant internal RNA modification in eukaryotic cells. m6A modifications affect multiple aspects of RNA metabolism, and m6A methylation has been shown to play a critical role in the progression of multiple cancers through a variety of mechanisms. This review summarizes the mechanisms by which m6A RNA methylation induced peripheral cancer cell progression and its potential role in the infiltration of immune cell of the glioblastoma microenvironment and novel immunotherapy. Assessing the pattern of m6A modification in glioblastoma will contribute to improving our understanding of microenvironmental infiltration and novel immunotherapies, and help in developing immunotherapeutic strategies.
    Keywords:  GBM; cancer progression; immunotherapy; m6A; stem cells
    DOI:  https://doi.org/10.3389/fimmu.2022.917153
  2. Methods Mol Biol. 2022 ;2528 329-344
    Detecting and Mapping N6-Methyladenosine on RNA/DNA Hybrids.
    Abdulkadir Abakir, Fahad Alenezi, Alexey Ruzov.
      N6-methyladenosine (m6A) is an RNA modification essential for posttranscriptional regulation of gene expression in eukaryotes. We recently demonstrated that m6A decorates the RNA components of R-loops, specific nucleic acid structures consisting of an RNA/DNA hybrid and a single strand of non-template DNA, that represent a major source of genetic instability and, at the same time, contribute to regulation of gene expression in mammalian cells. According to growing body of experimental evidence, adenosine methylation affects stability of these structures and potentially influences various aspects of their metabolism. Here, we present two methods for detection and analysis of m6A-containing RNA/DNA hybrids: an immunostaining protocol allowing investigation of their spatial distribution in eukaryotic cells and m6A-DNA immunoprecipitation (DIP), an antibody-based technique that permits their genome mapping and locus-specific analysis. In addition to the m6A-focused studies, these methodologies can also contribute to elucidating the functional roles of other RNA modifications in R-loop biology.
    Keywords:  Genome mapping techniques; Immunostaining; N6-methyladenosine; R-loops; RNA modifications; RNA/DNA hybrids; RNase H
    DOI:  https://doi.org/10.1007/978-1-0716-2477-7_22
  3. Front Immunol. 2022 ;13 897487
    METTL3-Mediated N6-Methyladenosine Modification of Trim59 mRNA Protects Against Sepsis-Induced Acute Respiratory Distress Syndrome.
    Yi Chen, Yuling Wu, Linjie Zhu, Caiyang Chen, Saihong Xu, Dan Tang, Yingfu Jiao, Weifeng Yu.
      N6-methyladenosine (m6A) RNA modification is a fundamental determinant of mRNA metabolism in eukaryotic cells and is involved in numerous physiological and pathological processes. However, the specific role of m6A modification in sepsis-induced acute respiratory distress syndrome(ARDS) remains unknown. Here, we show that the levels of m6A RNA were significantly decreased in septic lungs and that METTL3 was the main regulator involved in the absence of m6A RNA modification. Pulmonary endothelial barrier damage is a critical process in the pathogenesis of acute lung injury during sepsis. METTL3 regulated endothelial barrier dysfunction and inflammatory responses in sepsis-induced ARDS in vivo and in vitro. Furthermore, we identified tripartite motif-containing (Trim)59 as a key m6A effector and Trim59 deficiency exacerbated lung injury. Mechanistically, METTL3 inhibited endothelial injury in sepsis-induced ARDS through Trim59-associated NF-κB inactivation. Our findings revealed novel insights into epitranscriptional mechanisms in sepsis-induced ARDS via m6A modifications, which has important application value in the diagnosis, prognosis, and molecular-targeted therapy of sepsis-associated lung injury.
    Keywords:  METTL3; acute lung injury; endothelial barrier; epigenetic regulation; m6A; sepsis
    DOI:  https://doi.org/10.3389/fimmu.2022.897487
  4. BMC Biol. 2022 Jun 13. 20(1): 140
    Mettl14-mediated m6A modification is essential for visual function and retinal photoreceptor survival.
    Yeming Yang, Ping Shuai, Xiao Li, Kuanxiang Sun, Xiaoyan Jiang, Wenjing Liu, Weidong Le, Haisong Jiang, Yuping Liu, Xianjun Zhu.
       BACKGROUND: As the most abundant epigenetic modification of eukaryotic mRNA, N6-methyladenosine (m6A) modification has been shown to play a role in mammalian nervous system development and function by regulating mRNA synthesis and degeneration. However, the role of m6A modification in retinal photoreceptors remains unknown.
    RESULTS: We generated the first retina-specific Mettl14-knockout mouse models using the Rho-Cre and HRGP-Cre lines and investigated the functions of Mettl14 in retinal rod and cone photoreceptors. Our data showed that loss of Mettl14 in rod cells causes a weakened scotopic photoresponse and rod degeneration. Further study revealed the ectopic accumulation of multiple outer segment (OS) proteins in the inner segment (IS). Deficiency of Mettl14 in cone cells led to the mislocalization of cone opsin proteins and the progressive death of cone cells. Moreover, Mettl14 depletion resulted in drastic decreases in METTL3/WTAP levels and reduced m6A methylation levels. Mechanistically, transcriptomic analyses in combination with MeRIP-seq illustrated that m6A depletion via inactivation of Mettl14 resulted in reduced expression levels of multiple phototransduction- and cilium-associated genes, which subsequently led to compromised ciliogenesis and impaired synthesis and transport of OS-residing proteins in rod cells.
    CONCLUSIONS: Our data demonstrate that Mettl14 plays an important role in regulating phototransduction and ciliogenesis events and is essential for photoreceptor function and survival, highlighting the importance of m6A modification in visual function.
    Keywords:  Ciliogenesis; METTL14; N6-methyladenosine; Photoreceptor degeneration; Phototransduction
    DOI:  https://doi.org/10.1186/s12915-022-01335-x
  5. Gastroenterology. 2022 Jun 11. pii: S0016-5085(22)00629-1. [Epub ahead of print]
    METTL3 inhibits anti-tumor immunity by targeting m6A-BHLHE41-CXCL1/CXCR2 axis to promote colorectal cancer.
    Huarong Chen, Yasi Pan, Qiming Zhou, Cong Liang, Chi-Chun Wong, Yunfei Zhou, Dan Huang, Weixin Liu, Jianning Zhai, Hongyan Gou, Hao Su, Xiaoting Zhang, Hongzhi Xu, Yifei Wang, Wei Kang, William Ka Kei Wu, Jun Yu.
       BACKGROUND & AIMS: N6-Methyladenosine (m6A) is the most prevalent RNA modification and recognized as an important epitranscriptomic mechanism in colorectal cancer (CRC). We aim to exploit whether and how tumor-intrinsic m6A modification drove by methyltransferase like 3 (METTL3) can dictate the immune landscape of CRC.
    METHODS: Mettl3 knockout mice, CD34+ humanized mice and different syngeneic mice models were employed. Immune cells composition and cytokines level were analyzed by flow cytometry and Cytokine 23-Plex immunoassay, respectively. M6A-seq and RNA-seq were performed to identify downstream targets and pathways of METTL3. Human CRC specimens (n=176) were used to evaluate correlation between METTL3 expression and myeloid-derived suppressor cells (MDSCs) infiltration.
    RESULTS: We demonstrated that silencing of METTL3 in CRC cells reduced MDSCs accumulation to sustain activation and proliferation of CD4+ and CD8+ T cell, and eventually suppressed CRC in ApcMin/+Mettl3+/- mice, CD34+ humanized mice and syngeneic mice models. Mechanistically, METTL3 activated m6A-BHLHE41-CXCL1 axis by analysis of m6A-seq, RNA-seq and cytokines arrays. METTL3 promoted BHLHE41 expression in m6A-dependent manner, which subsequently induced CXCL1 transcription to enhance MDSC migration in vitro. However, the effect was negligible upon BHLHE41 depletion, CXCL1 protein or CXCR2 inhibitor SB265610 administration, inferring that METTL3 promotes MDSC migration via BHLHE41-CXCL1/CXCR2. Consistently, depletion of MDSCs by anti-Gr1 antibody or SB265610 blocked tumor-promoting effect of METTL3 in vivo. Importantly, targeting METTL3 by METTL3-sgRNA or specific inhibitor potentiated the effect of anti-PD1 treatment.
    CONCLUSIONS: Our study identifies METTL3 as a potential therapeutic target for CRC immunotherapy whose inhibition reverses immune suppression through m6A-BHLHE41-CXCL1 axis. METTL3 inhibition plus anti-PD-1 treatment show promising antitumor efficacy against CRC.
    Keywords:  Colorectal cancer; MDSC; METTL3; N(6)-Methyladenosine; immunotherapy
    DOI:  https://doi.org/10.1053/j.gastro.2022.06.024
  6. J Immunol Res. 2022 ;2022 8766735
    Characterization of m6A Methylation Modification Patterns in Colorectal Cancer Determines Prognosis and Tumor Microenvironment Infiltration.
    Qingfang Yue, Yuan Zhang, Fei Wang, Fei Cao, Jun Bai, Xianglong Duan.
      Cumulative studies have suggested that dysregulation of m6A regulators and immunity is highly linked to the prognosis of patients with cancer. However, the potential contribution of m6A modification patterns to the tumor microenvironment (TME) and the therapeutic efficacy of immunotherapy for colorectal cancer (CRC) remain elusive. A comprehensive analysis of the m6A modification profiles of 458 patients with CRC was performed by clustering 21 genes encoding m6A methylation regulators and linking the m6A modification pattern with TME characteristics. Using principal component analysis (PCA), a risk model was constructed to quantify individual m6A modification patterns in patients with CRC. The results indicated that the expression profiles and genetic mutations of 21 genes encoding m6A methylation regulators in CRC were characterized by a high degree of heterogeneity. Three m6A clusters had significant differences in prognosis, m6A modification patterns, and TME characteristics. Furthermore, a risk model, termed m6Ascore, was developed by PCA to quality m6A methylation patterns at an individual level. The m6Ascore could stratify patients into high- and low-m6Ascore groups. Further analyses demonstrated that the m6Ascore had a good predictive performance for overall survival and clinical efficacy of immunotherapy in patients with CRC. Finally, the predictive value of the model was validated by external cohorts. In conclusion, the comprehensive characterization of m6A methylation modification patterns might contribute to our understanding of the TME in CRC and the development of personalized antitumor immunotherapy in the future.
    DOI:  https://doi.org/10.1155/2022/8766735
  7. ACS Chem Biol. 2022 Jun 15.
    YTHDF3 Facilitates eIF2AK2 and eIF3A Recruitment on mRNAs to Regulate Translational Processes in Oxaliplatin-Resistant Colorectal Cancer.
    Yang Zhao, Hongchao Zhao, Danhuan Zhang, Qiuying Quan, Yan Ge, Liantao Li, Lingchuan Guo.
      Oxaliplatin, as a first-line drug, frequently causes chemo-resistance in colorectal cancer (CRC). The role of N6-methyladenosine (m6A) modification in multiple biological functions has been well studied. However, the molecular mechanisms underlying m6A methylation in modulating anti-cancer drug resistance in CRC remain obscure. In the present study, we found that YTH m6A RNA-binding protein 3 (YTHDF3) was highly expressed in oxaliplatin-resistant (OXAR) CRC tissues and cells. Moreover, we observed that YTHDF3 could recognize the 5' untranslated region of significantly m6A-methylated RNAs, which were associated with tumor resistance and recruit eukaryotic translation initiation factor 3 subunit A (eIF3A) to facilitate the translation of these target genes. Furthermore, we determined that eukaryotic translation initiation factor 2 alpha kinase 2 (eIF2AK2) bridged YTHDF3 and eIF3A, enhancing the stability of the YTHDF3/eIF3A complex in OXAR CRC cells. Taken together, our data identified YTHDF3 as a novel hallmark and revealed the molecular mechanism of YTHDF3 on gene translation via coordination with eIF2AK2 in OXAR CRC cells.
    DOI:  https://doi.org/10.1021/acschembio.2c00131
  8. Clin Transl Med. 2022 Jun;12(6): e848
    YTHDF2 promotes intrahepatic cholangiocarcinoma progression and desensitises cisplatin treatment by increasing CDKN1B mRNA degradation.
    Chen-Song Huang, Ying-Qin Zhu, Qiong-Cong Xu, Siyun Chen, Yue Huang, Guangyin Zhao, Xuhao Ni, Bo Liu, Wei Zhao, Xiao-Yu Yin.
       BACKGROUND: Intrahepatic cholangiocarcinoma (ICC) is an aggressive cancer with exceedingly poor prognosis, and chemoresistance is a huge challenge for treatment. N6-methyladenosine (m6 A) modification plays an important role in the progression and chemoresistance of cancers. We aimed to investigate the oncogenic function and therapeutic significance of the m6 A binding protein, YTH domain family 2 (YTHDF2), in ICC progression and cisplatin-based chemotherapy.
    METHODS: Several independent data sets were used to assess the expression of YTHDF2 in ICC, particularly in chemoresistant ICC. Knockdown and overexpression were used to evaluate the effects of YTHDF2 on tumourigenesis and cisplatin response in ICC. Multi-omics sequencing was performed to identify target genes. RIP, dual luciferase reporter, RNA stability experiment and loss-of-function assays were conducted to study the mechanisms underlying the oncogenic function of YTHDF2. Furthermore, patient-derived xenograft (PDX) model was established to determine the effect of combination treatment of YTHDF2 siRNA and cisplatin in ICC.
    RESULTS: Our study showed that YTHDF2 was upregulated in ICC tissues, particularly in chemoresistant ICC tissues, and correlated with poor prognosis. Furthermore, silencing YTHDF2 led to inhibited proliferation, promoted apoptosis and G0/G1 cell cycle arrest. Its downregulation also enhanced DNA damage and sensitised ICC cells to cisplatin. YTHDF2 overexpression exerted the opposite results. Integration analysis using RNA-seq, MeRIP-seq and anti-YTHDF2 RIP-seq elucidated the role of YTHDF2 in tumourigenesis and cisplatin-desensitising function by promoting the degradation of cyclin-dependent kinase inhibitor 1B (CDKN1B) mRNA in an m6 A-dependent manner. Downregulation of CDKN1B increased the YTHDF2 silencing-induced influence on tumourigenesis and cisplatin response to ICC. In addition, the combination treatment of YTHDF2 siRNA and cisplatin significantly enhanced the anti-tumour effect of cisplatin in a chemoresistant ICC PDX model.
    CONCLUSIONS: YTHDF2 exhibits tumour oncogenic and cisplatin-desensitising properties, which may offer insight into the development of novel combination therapeutic strategies for ICC.
    Keywords:  YTHDF2; cisplatin-resistance; intrahepatic cholangiocarcinoma; tumourigenensis
    DOI:  https://doi.org/10.1002/ctm2.848
  9. Mol Plant Pathol. 2022 Jun 14.
    AlkB RNA demethylase homologues and N6 -methyladenosine are involved in Potyvirus infection.
    Jianying Yue, Yao Wei, Zhenqi Sun, Yahan Chen, Xuefeng Wei, Haijuan Wang, Fabio Pasin, Mingmin Zhao.
      Proteins of the alkylation B (AlkB) superfamily show RNA demethylase activity removing methyl adducts from N6 -methyladenosine (m6 A). m6 A is a reversible epigenetic mark of RNA that regulates human virus replication but has unclear roles in plant virus infection. We focused on Potyvirus-the largest genus of plant RNA viruses-and report here the identification of AlkB domains within P1 of endive necrotic mosaic virus (ENMV) and an additional virus of a putative novel species within Potyvirus. We show that Nicotiana benthamiana m6 A levels are reduced by infection of plum pox virus (PPV) and potato virus Y (PVY). The two potyviruses lack AlkB and the results suggest a general involvement of RNA methylation in potyvirus infection and evolution. Methylated RNA immunoprecipitation sequencing of virus-infected samples showed that m6 A peaks are enriched in plant transcript 3' untranslated regions and in discrete internal and 3' terminal regions of PPV and PVY genomes. Down-regulation of N. benthamiana AlkB homologues of the plant-specific ALKBH9 clade caused a significant decrease in PPV and PVY accumulation. In summary, our study provides evolutionary and experimental evidence that supports the m6 A implication and the proviral roles of AlkB homologues in Potyvirus infection.
    Keywords:   Potyvirus ; N6-methyladenosine (m6A); RNA methylation; alkylation B (AlkB); endive necrotic mosaic virus (ENMV); plant-virus interaction
    DOI:  https://doi.org/10.1111/mpp.13239
  10. Hepatology. 2022 Jun 14.
    METTL1 is required for non-homologous end joining repair and renders hepatocellular carcinoma resistant to radiotherapy.
    Junbin Liao, Yang Yi, Xin Yue, Xiaoxue Wu, Meiyan Zhu, Yong Chen, Sui Peng, Ming Kuang, Shuibin Lin, Zhenwei Peng.
       BACKGROUND & AIMS: Radiotherapy is an increasingly essential therapeutic strategy in the management of hepatocellular carcinoma (HCC). Nevertheless, resistance to radiotherapy is one of the primary obstacles to successful treatment outcomes. Hence, we aim to elucidate the mechanisms underlying radioresistance and identify reliable biotargets that would be inhibited to enhance the efficacy of radiotherapy in HCC.
    APPROACH & RESULTS: From a label-free quantitative proteome screening, we identified tRNA (guanine-N (7)-) methyltransferase1 (METTL1), a key enzyme for m7 G tRNA modification, as an essential driver for HCC cells radioresistance. We reveal that METTL1 promotes DNA DSB repair and renders HCC cells resistant to ionizing radiation (IR) using loss- and gain-of-function assays in vitro and in vivo. Mechanistically, METTL1-mediated m7 G tRNA modification selectively regulates the translation of DNA-PKcs or DNA ligase IV with higher frequencies of m7 G-related codons after IR treatment, thereby resulting in the enhancement of NHEJ-mediated DNA DSB repair efficiency. Clinically, high METTL1 expression in tumor tissue is significantly correlated with poor prognosis in radiotherapy-treated HCC patients.
    CONCLUSIONS: Our findings show that METTL1 is a critical enhancer for HCC cell NHEJ-based DNA repair following IR therapy. These findings give novel insights into the role of tRNA modification in mRNA translation control in HCC radioresistance.
    DOI:  https://doi.org/10.1002/hep.32615
  11. Front Oncol. 2022 ;12 882292
    Comprehensive Analysis of the Function, Immune Profiles, and Clinical Implication of m1A Regulators in Lung Adenocarcinoma.
    Guangyao Bao, Tian Li, Xiaojiao Guan, Yao Yao, Jie Liang, Yifang Xiang, Xinwen Zhong.
       Background: Previous studies have demonstrated that transcriptional RNA methyladenosine modification significantly affects tumor initiation and progression. However, clinical implications of N1-methyladenosine (m1A) regulators and their effect on tumor immunity in lung adenocarcinoma (LUAD) are still poorly elucidated.
    Methods: Herein, the characteristics of somatic mutation, copy number variation (CNV), DNA methylation, and expression levels of m1A regulators were thoroughly analyzed. We classified 955 lung adenocarcinoma patients into different m1A modification patterns based on an unsupervised consensus clustering algorithm. We then calculated the differences in gene expression, prognosis outcomes, and immune profiles among different m1A clusters. Subsequently, we screened differently expressed genes (DEGs) related to prognosis among different m1A clusters. We identified m1A related gene clusters according to the prognosis-related different expressed genes. We further constructed a scoring standard named the m1A score and comprehensively analyzed the survival outcomes, clinical-pathological features, immune microenvironment, treatment responses of immunotherapy, and drug susceptibility in different m1A score groups.
    Results: In total, three different m1A modification patterns were identified, which contained cluster A, B, and C. Among them, cluster A processed the poorest clinical outcomes, the lowest immune cell infiltration rate, and the highest tumor purity score. Then, three m1A gene clusters (gene cluster A, B, C) were speculated. Subsequently, we combined m1A modification patterns and m1A gene cluster to classify lung adenocarcinoma patients into high and low m1A score groups. The low m1A score group was accompanied by higher mortality, higher tumor mutation burden (TMB) and genome mutation frequency, and lower programmed cell death-Ligand 1 (PD-L1) expression and tumor immune dysfunction and exclusion (TIDE) expression. Moreover, the m1A score exhibited positive correlation with almost all immune cells. Finally, common chemotherapeutic and targeted therapy agents exhibited obvious differences in drug susceptibility in different m1A score groups.
    Conclusions: Collectively, we explored the potential value of m1A regulators in the prognosis and treatment of lung adenocarcinoma in multiple dimensions and provided some preliminary basis for the follow-up study of m1A regulators in lung adenocarcinoma.
    Keywords:  immune microenvironment; immunotherapy; lung adenocarcinoma; m1A; prognosis
    DOI:  https://doi.org/10.3389/fonc.2022.882292
  12. Front Genet. 2022 ;13 903117
    An m6A/m5C/m1A/m7G-Related Long Non-coding RNA Signature to Predict Prognosis and Immune Features of Glioma.
    Dongqi Shao, Yu Li, Junyong Wu, Binbin Zhang, Shan Xie, Xialin Zheng, Zhiquan Jiang.
      Background: Gliomas are the most common and fatal malignant type of tumor of the central nervous system. RNA post-transcriptional modifications, as a frontier and hotspot in the field of epigenetics, have attracted increased attention in recent years. Among such modifications, methylation is most abundant, and encompasses N6-methyladenosine (m6A), 5-methylcytosine (m5C), N1 methyladenosine (m1A), and 7-methylguanosine (m7G) methylation. Methods: RNA-sequencing data from healthy tissue and low-grade glioma samples were downloaded from of The Cancer Genome Atlas database along with clinical information and mutation data from glioblastoma tumor samples. Forty-nine m6A/m5C/m1A/m7G-related genes were identified and an m6A/m5C/m1A/m7G-lncRNA signature of co-expressed long non-coding RNAs selected. Least absolute shrinkage and selection operator Cox regression analysis was used to identify 12 m6A/m5C/m1A/m7G-related lncRNAs associated with the prognostic characteristics of glioma and their correlation with immune function and drug sensitivity analyzed. Furthermore, the Chinese Glioma Genome Atlas dataset was used for model validation. Results: A total of 12 m6A/m5C/m1A/m7G-related genes (AL080276.2, AC092111.1, SOX21-AS1, DNAJC9-AS1, AC025171.1, AL356019.2, AC017104.1, AC099850.3, UNC5B-AS1, AC006064.2, AC010319.4, and AC016822.1) were used to construct a survival and prognosis model, which had good independent prediction ability for patients with glioma. Patients were divided into low and high m6A/m5C/m1A/m7G-LS groups, the latter of which had poor prognosis. In addition, the m6A/m5C/m1A/m7G-LS enabled improved interpretation of the results of enrichment analysis, as well as informing immunotherapy response and drug sensitivity of patients with glioma in different subgroups. Conclusion: In this study we constructed an m6A/m5C/m1A/m7G-LS and established a nomogram model, which can accurately predict the prognosis of patients with glioma and provides direction toward promising immunotherapy strategies for the future.
    Keywords:  M6A; RNA methylation; glioma; long non-coding RNA; m1B; m5C; m7G; prognostic signature
    DOI:  https://doi.org/10.3389/fgene.2022.903117
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