Detection of N6‑methyladenosine modification residues (Review)

Zhu, Wei; Wang, Jingzi; Xu, Zhi‐Qiang; Cao, Mengda; Hu, Qiaoli; Chen, Pan; Guo, Miao; Wei, Ji‐Fu; Yang, Haiwei

doi:10.3892/ijmm.2019.4169

Cited by 42 publications

(46 citation statements)

References 79 publications

(150 reference statements)

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“…The ultimate message we get from all these recent papers about epitranscriptomic modifications in glioma is that we are likely observing only the tip of the iceberg, and we will surely find many more sophisticated mechanisms which can finely modulate transcript fate in glioma cells. As the techniques employed to analyzeepitranscriptomic modifications become more and more refined [65,66], we become able to detect subtle changes even in little portions of the transcripts, as clearly shown in the case of the unique cytosine methylation event in 28S rRNA by NSUN5. As Janin's paper teaches, a single, tiny change in one nucleotide of a single type of RNA can dramatically change a cell's fate [55].…”

Section: Glioblastoma Stem Cells and U87 Glioblastoma Cell Linementioning

confidence: 92%

Insights into the Regulatory Role of m6A Epitranscriptome in Glioblastoma

Galardi

Michienzi

Ciafrè

2020

IJMS

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N6-methyladenosine (m6A) is one of the most widespread and abundant internal messenger RNA modifications found in eukaryotes. Emerging evidence suggests that this modification is strongly linked to the activation and inhibition of cancer pathways and is associated with prognostically significant tumour subtypes. The present review describes the dynamic nature of m6A regulator enzymes, as methyltransferases, demethylases and m6A binding proteins, and points out thevalue of the balance among these proteins in regulating gene expression, cell metabolism and cancer development. The main focus of this review is on the roles of m6A modification in glioblastoma, the most aggressive and invariably lethal brain tumour. Although the study of m6A in glioblastoma is a young one, and papers in this field can yield divergent conclusions, the results collected so far clearly demonstrate that modulation of mRNA m6A levels impacts multiple aspects of this tumour, including growth, glioma stem cells self-renewal, and tumorigenesis, suggesting that mRNA m6A modification may serve as a promising target for glioblastoma therapy. We also present recent data about another type of epitranscriptomic modification, the methylation of cytosine at a specific site of 28S rRNA, as it was recently shown to affect the biology of glioma cells, with high potential of clinical implications.

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Section: Glioblastoma Stem Cells and U87 Glioblastoma Cell Linementioning

confidence: 92%

Insights into the Regulatory Role of m6A Epitranscriptome in Glioblastoma

Galardi

Michienzi

Ciafrè

2020

IJMS

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“…Currently, a massive number of technologies have been developed for m 6 A detection based on the immunohistochemistry or hybridization properties ( Ovcharenko and Rentmeister, 2018 ). According to their detection performance, these technologies can be classified into the semiquantitative, quantitative, and precise location detection methods ( Zhu et al, 2019 ; Table 1 ).…”

Section: Advances In Technologies For M 6 a Detectmentioning

confidence: 99%

Multifaceted Functions and Novel Insight Into the Regulatory Role of RNA N6-Methyladenosine Modification in Musculoskeletal Disorders

Zhang

Liu

et al. 2020

Front. Cell Dev. Biol.

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RNA modifications have emerged as key regulators of transcript expression in diverse physiological and pathological processes. As one of the most prevalent types of RNA modifications, N 6 -methyladenosine (m 6 A) has become the highlight in modulation of various diseases through interfering RNA splicing, translation, nuclear export, and decay. In many cases, the detailed functions of m 6 A in cellular processes and diseases remain unclear. Notably, recent studies have determined the relationship between m 6 A modification and musculoskeletal disorders containing osteosarcoma, osteoarthritis, rheumatoid arthritis, osteoporosis, etc. Herein, this review comprehensively summarizes the recent advances of m 6 A modification in pathogenesis and progression of musculoskeletal diseases. Specifically, the underlying molecular mechanisms, detection technologies, regulatory functions, clinical implications, and future perspectives of m 6 A in musculoskeletal disorders are discussed, with the aim to provide a novel insight into their association.

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“…Among these, m6A modification is the most prevalent one in eukaryotes, which occurs in mammalian mRNAs, long noncoding RNAs, micro RNAs, involving in many RNA functions such as mRNA stability, splicing, transport, localization and translation, primary microRNA processing and RNA‐protein interactions . The levels of m6A modification in mRNAs were usually controlled by so‐called ‘reader’, ‘writer’ and ‘eraser’ . The ‘writer’, which is a high conserved methylase complex, containing methyltransferase like 3 (METTL3), methyltransferase like 14, Wilms’ tumour 1‐associating protein, RNA‐binding motif protein 15, Vir like m6A methyltransferase associated, Fl(2)d‐associated complex component and Hakai…”

Section: Introductionmentioning

confidence: 99%

“…15 The levels of m6A modification in mRNAs were usually controlled by so-called 'reader', 'writer' and 'eraser'. 16,17 The 'writer', which is a high conserved methylase complex, containing methyltransferase like 3 (METTL3), 18 methyltransferase like 14, 18 Wilms' tumour 1-associating protein, 19 RNA-binding motif protein 15,20,21 Vir like m6A methyltransferase associated, 18,22 Fl(2)d-associated complex component 20 and Hakai. 23 Recent studies showed that m6A modification played essential roles in tissue development, stem cell formation and differentiation, 24,25 control of heat shock response 26 and circadian clock controlling, 27 as well as in tumours formation.…”

Section: Introductionmentioning

confidence: 99%

Methyltransferase like 3 promotes colorectal cancer proliferation by stabilizing CCNE1 mRNA in an m6A‐dependent manner

Zhu

et al. 2020

J Cellular Molecular Medi

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m6A modification is the most prevalent RNA modification in eukaryotes. As the critical N6‐methyladenosine (m6A) methyltransferase, the roles of methyltransferase like 3 (METTL3) in colorectal cancer (CRC) are controversial. Here, we confirmed that METTL3, a critical m6A methyltransferase, could facilitate CRC progression in vitro and in vivo. Further, we found METTL3 promoted CRC cell proliferation by methylating the m6A site in 3′‐untranslated region (UTR) of CCNE1 mRNA to stabilize it. Moreover, we found butyrate, a classical intestinal microbial metabolite, could down‐regulate the expression of METTL3 and related cyclin E1 to inhibit CRC development. METTL3 promotes CRC proliferation by stabilizing CCNE1 mRNA in an m6A‐dependent manner, representing a promising therapeutic strategy for the treatment of CRC.

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Detection of N6‑methyladenosine modification residues (Review)

Cited by 42 publications

References 79 publications

Insights into the Regulatory Role of m6A Epitranscriptome in Glioblastoma

Insights into the Regulatory Role of m6A Epitranscriptome in Glioblastoma

Multifaceted Functions and Novel Insight Into the Regulatory Role of RNA N6-Methyladenosine Modification in Musculoskeletal Disorders

Methyltransferase like 3 promotes colorectal cancer proliferation by stabilizing CCNE1 mRNA in an m6A‐dependent manner

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