RNA N1-methyladenosine regulator-mediated methylation modification patterns and heterogeneous signatures in glioma

Mao, Meng; Chu, Qinjun; Lou, Yongli; Lv, Peipei; Wang, Linjian

doi:10.3389/fimmu.2022.948630

Cited by 10 publications

(5 citation statements)

References 43 publications

(48 reference statements)

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“…Discussion m 1 A reportedly plays a pivotal role in various functional activities and has recently drawn increasing attention. Many bioinformatics analyses have suggested that m 1 A-regulating genes play essential roles in different tumors [17][18][19][27][28][29]. However, the impact of m 1 A on BLCA remains poorly known.…”

Section: Nf-κb Promotes Trmt61a Gene Transcription and Induces Nuclea...mentioning

confidence: 99%

“…Recent studies revealed that alterations in m 1 A regulators are closely associated with multiple tumors [15][16][17][18][19][20][21][22]. For instance, the expression of TRMT6 and TRMT61A is signi cantly increased in hepatocellular carcinoma tissues, and the increased TRMT6 and TRMT61A levels are negatively associated with patient prognosis [21].…”

Section: Introductionmentioning

confidence: 99%

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N1-methyladenosine methylation in mRNAs drives bladder cancer progression

Song

Yin²,

Fan

et al. 2023

Preprint

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With the growing recognition of RNA modification as a hallmark of cancer, N1-methyladenosine (m1A) methylation has been reported as a key mechanism of post-transcriptional regulation. However, the molecular mechanisms underlying m1A modification in bladder cancer (BLCA) progression remain unclear. In the current study, we aimed to explore the role of m1A methylation in BLCA. We found that the expression of the m1A methyltransferase TRMT61A was significantly elevated in human BLCA tissues. TRMT61A inhibition attenuated BLCA cell proliferation, migration, and invasion in vitro and tumor growth in vivo. Mechanistically, transcriptional profiling identified heme oxygenase-2 (HMOX2) as an m1A modification target of TRMT61A, and HMOX2 mRNA m1A modifications were reduced in TRMT61A-deficient cells. TRMT61A promoted HMOX2 mRNA stabilization in a YTHDF1-dependent manner, and YTHDF1 knockdown decreased the stability of HMOX2 mRNA through an m1A modification-dependent mechanism, leading to the inhibition of tumor cell proliferation. Moreover, NF-κB was found to bind to the promoter region of TRMT61A and stimulate its expression. NF-κB activation also increased the nuclear translocation of TRMT61A. Together, our results demonstrate the oncogenic role of TRMT61A and the m1A modification-mediated NF-κB/TRMT61A/HMOX2 signaling pathway activation in BLCA, thus highlighting a novel therapeutic target for this disease.

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Section: Nf-κb Promotes Trmt61a Gene Transcription and Induces Nuclea...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

N1-methyladenosine methylation in mRNAs drives bladder cancer progression

Song

Yin²,

Fan

et al. 2023

Preprint

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“…3.4 Other RNA modifications and smallmolecule regulators Mao et al (2022) constructed a signature based on m1A regulators with The Chinese Glioma Genome Atlas (CGGA) and The Cancer Genome Atlas (TCGA) datasets, which divided gliomas into different subtypes. Four m1A modification-related patterns were found, with different prognoses.…”

Section: The Potential Regulatory Mechanisms Of A-to-i Rna Editing In...mentioning

confidence: 99%

The role of RNA modification in the generation of acquired drug resistance in glioma

Wei

Long

et al. 2022

Front. Genet.

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Glioma is the most common malignant tumor in the central nervous system. The clinical treatment strategy is mainly surgery combined with concurrent temozolomide chemotherapy, but patients can develop drug resistance during treatment, which severely limits its therapeutic efficacy. Epigenetic regulation at the RNA level is plastic and adaptable, and it can induce a variety of tumor responses to drugs. The regulators of RNA modification include methyltransferases, demethylases, and methylation binding proteins; these are also considered to play an important role in the development, prognosis, and therapeutic response of gliomas, which provides a basis for finding new targets of epigenetic drugs and resetting the sensitivity of tumor cells to temozolomide. This review discusses the relationship between the development of adaptive drug resistance and RNA modification in glioma and summarizes the progress of several major RNA modification strategies in this field, especially RNA m6A modification, m5C modification, and adenosine-to-inosine editing.

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“…As a particularly important epigenetic modification, RNA methylation plays a key role in the regulation of tissue-specific gene expression (4, 5). Recent evidence has demonstrated that the expression of tumor-related genes is controlled by RNA regulators, which have a considerable impact on the formation and progression of cancers (6, 7). However, the roles of RNA regulators in COPD are yet to be explored.…”

Section: Introductionmentioning

confidence: 99%

Combining Bulk and Single-Cell RNA Sequencing Data to Identify RNA methylation and Autophagy-Related Signatures in Patients with Chronic Obstructive Pulmonary Disease

Liao,

Zhang,

Wang

et al. 2023

Preprint

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Background: Chronic Obstructive Pulmonary Disease (COPD) is a heterogeneous lung condition associated with RNA methylation and autophagy. However, the specific autophagy-related genes and RNA methylation regulators involved in COPD development remain unknown. Methods: We analyzed COPD and non-COPD patients datasets obtained from the Gene Expression Omnibus database, including Tissue Sequencing Transcriptome (bulk-seq) and single-cell sequencing (scRNA-seq) data. Differentially expressed genes (DEGs) were identified through differential genetic analysis using non-COPD bulk-seq data as the control group and COPD samples were used as the experimental group. Animal experiments were conducted to validate the expression of key genes. COPD model mice were exposed to smoke for four months, and lung function and histopathological changes were assessed. The mRNA and protein expression levels of FTO, IGF2BP2, DDIT3, DNAJB1, and YTHDF3 were measured using RT-qPCR and Western blotting, respectively. Results: We identified FTO, IGF2BP2, and YTHDF3 as key methylation genes, along with autophagy hub genes;DDIT3 and DNAJB1. Animal experiments showed significantly increased mRNA and protein levels of FTO, YTHDF3 and DNAJB1 and significantly decreased levels of IGF2BP2 in lung tissue of COPD mice compared to the control group. Conclusion: Our findings suggest that DDIT3 and DNAJB1 as autophagy hub genes, along with FTO, IGF2BP2 and YTHDF3 as RNA methylation genes, may play crucial roles in the development of COPD. These findings, supported by bulk-seq and scRNA-seq data, contribute novel genetic evidence for understanding the epigenetics of COPD.

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RNA N1-methyladenosine regulator-mediated methylation modification patterns and heterogeneous signatures in glioma

Cited by 10 publications

References 43 publications

N1-methyladenosine methylation in mRNAs drives bladder cancer progression

N1-methyladenosine methylation in mRNAs drives bladder cancer progression

The role of RNA modification in the generation of acquired drug resistance in glioma

Combining Bulk and Single-Cell RNA Sequencing Data to Identify RNA methylation and Autophagy-Related Signatures in Patients with Chronic Obstructive Pulmonary Disease

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