Epitranscriptomic
            <i>N</i>
            <sup>6</sup>
            -Methyladenosine Profile of SARS-CoV-2-Infected Human Lung Epithelial Cells

Phillips, Stacia L.; Mishra, Tarun; Khadka, Shaubhagya; Bohan, Dana; Espada, Constanza E.; Maury, Wendy; Wu, Li

doi:10.1128/spectrum.03943-22

Cited by 7 publications

(4 citation statements)

References 52 publications

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“…m6A reader genes show uneven expression levels, suggesting that the stability of specific transcripts is usually restricted in AD brains [ 28 ]. Different patterns of these m6A regulators can lead to an aberrant post-transcriptional modification environment [ 29 ], which may alter the expression of AD-related genes. Specifically, we observed a significant downward trend in METTL3 in AD brain tissue.…”

Section: Discussionmentioning

confidence: 99%

An Exploration of the Coherent Effects between METTL3 and NDUFA10 on Alzheimer’s Disease

Yang

Pang

Guo

et al. 2023

IJMS

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Alzheimer’s disease (AD) is a neurodegenerative disorder characterized primarily by a decline in cognitive function. However, the etiopathogenesis of AD is unclear. N6-methyladenosine (m6A) is abundant in the brain, and it is interesting to explore the relationship between m6A and AD causes. In this paper, the gene expression of METTL3 and NDUFA10 were found to correlate with the Mini-mental State Examination (MMSE), which is a clinical indicator of the degree of dementia. METTL3 is involved in post-transcriptional methylation and the formation of m6A. NDUFA10 encodes the protein with NADH dehydrogenase activity and oxidoreductase activity in the mitochondrial electron transport chain. The following three characteristics were observed in this paper: 1. The lower the expression level of NDUFA10, the smaller the MMSE, and the higher the degree of dementia. 2. If the expression level of METTL3 dropped below its threshold, the patient would have a risk of AD with a probability close to 100%, suggesting a basic necessity for m6A to protect mRNA. 3. The lower the expression levels of both METTL3 and NDUFA10, the more likely the patient would suffer from AD, implying the coherence between METTL3 and NDUFA10. Regarding the above discovery, the following hypothesis is presented: METTL3 expression level is downregulated, then the m6A modification level of NDUFA10 mRNA is also decreased, thereby reducing the expression level of NDUFA10-encoded protein. Furthermore, the abnormal expression of NDUFA10 contributes to the assembly disorder of mitochondrial complex I and affects the process of the electron respiratory chain, with the consequent development of AD. In addition, to confirm the above conclusions, the AI Ant Colony Algorithm was improved to be more suitable for discovering the characteristics of AD data, and the SVM diagnostic model was applied to mine the coherent effects on AD between METTL3 and NDUFA10. In conclusion, our findings suggest that dysregulated m6A leads to altered expression of its target genes, thereby affecting AD’s development.

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Section: Discussionmentioning

confidence: 99%

An Exploration of the Coherent Effects between METTL3 and NDUFA10 on Alzheimer’s Disease

Yang

Pang

Guo

et al. 2023

IJMS

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“…The nutritional availability of cancer cells in the tumor micro-environment constantly changes during tumor progression, whereby they can utilize abundant lipids to promote rapid cell growth [ 19 , 20 ]. Studies have shown that m6A modification dynamically changes with the external environment [ 21 , 22 ]. For instance, a high-fat environment can lead to changes in m6A-related molecules.…”

Section: Discussionmentioning

confidence: 99%

Down-regulated FTO and ALKBH5 co-operatively activates FOXO signaling through m6A methylation modification in HK2 mRNA mediated by IGF2BP2 to enhance glycolysis in colorectal cancer

Chen

et al. 2023

Cell Biosci

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Background N6-methyladenosine (m6A) modification is the most abundant reversible methylation modification in eukaryotes, and it is reportedly closely associated with a variety of cancers progression, including colorectal cancer (CRC). This study showed that activated lipid metabolism and glycolysis play vital roles in the occurrence and development of CRC. However, only a few studies have reported the biological mechanisms underlying this connection. Methods Protein and mRNA levels of FTO and ALKBH5 were measured using western blot and qRT-PCR. The effects of FTO and ALKBH5 on cell proliferation were examined using CCK-8, colony formation, and EdU assays, and the effects on cell migration and invasion were tested using a transwell assay. m6A RNA immunoprecipitation (MeRIP) and RNA-seq was used to explore downstream target gene. RIP was performed to verify the interaction between m6A and HK2. The function of FTO and ALKBH5 in vivo was determined by xenograft in nude mice. Results In this study, FTO and ALKBH5 were significantly down-regulated in CRC patients and cells both in vivo and in vitro in a high-fat environment. Moreover, FTO and ALKBH5 over-expression hampered cell proliferation both in vitro and in vivo. Conversely, FTO and ALKBH5 knockdown accelerated the malignant biological behaviors of CRC cells. The mechanism of action of FTO and ALKBH5 involves joint regulation of HK2, a key enzyme in glycolysis, which was identified by RNA sequencing and MeRIP-seq. Furthermore, reduced expression of FTO and ALKBH5 jointly activated the FOXO signaling pathway, which led to enhanced proliferation ability in CRC cells. IGF2BP2, as a m6A reader, positively regulated HK2 mRNA in m6A dependent manner. Additionally, down-regulation of FTO/ALKBH5 increased METTL3 and decreased METTL14 levels, further promoting CRC progression. Conclusion In conclusion, our study revealed the FTO-ALKBH5/IGF2BP2/HK2/FOXO1 axis as a mechanism of aberrant m6A modification and glycolysis regulation in CRC.

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“…More recently, Stacia et al. [ 69 ] defined the m 6 A modification profile in SARS-CoV-2-infected cells, identifying various mRNA and noncoding RNA species with differential m 6 A modifications, further enriching our understanding of the virus’s interaction with host cell mechanisms.…”

Section: Sars-cov-2 As a Paradigm For M 6 A Epitra...mentioning

confidence: 99%

Decoding epitranscriptomic regulation of viral infection: mapping of RNA N6-methyladenosine by advanced sequencing technologies

Fan,

Zhang,

Guo

et al. 2024

Cell Mol Biol Lett

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Elucidating the intricate interactions between viral pathogens and host cellular machinery during infection is paramount for understanding pathogenic mechanisms and identifying potential therapeutic targets. The RNA modification N6-methyladenosine (m6A) has emerged as a significant factor influencing the trajectory of viral infections. Hence, the precise and quantitative mapping of m6A modifications in both host and viral RNA is pivotal to understanding its role during viral infection. With the rapid advancement of sequencing technologies, scientists are able to detect m6A modifications with various quantitative, high-resolution, transcriptome approaches. These technological strides have reignited research interest in m6A, underscoring its significance and prompting a deeper investigation into its dynamics during viral infections. This review provides a comprehensive overview of the historical evolution of m6A epitranscriptome sequencing technologies, highlights the latest developments in transcriptome-wide m6A mapping, and emphasizes the innovative technologies for detecting m6A modification. We further discuss the implications of these technologies for future research into the role of m6A in viral infections. Graphical Abstract

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Epitranscriptomic N ⁶ -Methyladenosine Profile of SARS-CoV-2-Infected Human Lung Epithelial Cells

Cited by 7 publications

References 52 publications

An Exploration of the Coherent Effects between METTL3 and NDUFA10 on Alzheimer’s Disease

An Exploration of the Coherent Effects between METTL3 and NDUFA10 on Alzheimer’s Disease

Down-regulated FTO and ALKBH5 co-operatively activates FOXO signaling through m6A methylation modification in HK2 mRNA mediated by IGF2BP2 to enhance glycolysis in colorectal cancer

Decoding epitranscriptomic regulation of viral infection: mapping of RNA N6-methyladenosine by advanced sequencing technologies

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Epitranscriptomic N 6 -Methyladenosine Profile of SARS-CoV-2-Infected Human Lung Epithelial Cells

Cited by 7 publications

References 52 publications

An Exploration of the Coherent Effects between METTL3 and NDUFA10 on Alzheimer’s Disease

An Exploration of the Coherent Effects between METTL3 and NDUFA10 on Alzheimer’s Disease

Down-regulated FTO and ALKBH5 co-operatively activates FOXO signaling through m6A methylation modification in HK2 mRNA mediated by IGF2BP2 to enhance glycolysis in colorectal cancer

Decoding epitranscriptomic regulation of viral infection: mapping of RNA N6-methyladenosine by advanced sequencing technologies

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Epitranscriptomic N ⁶ -Methyladenosine Profile of SARS-CoV-2-Infected Human Lung Epithelial Cells