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Diagnosis and Pathobiology
Published in Franklyn De Silva, Jane Alcorn, The Elusive Road Towards Effective Cancer Prevention and Treatment, 2023
Franklyn De Silva, Jane Alcorn
The epigenetic machinery can be separated into a number of interconnected components such as histone PTMs, DNA methylation (the most well-studied epigenetic alteration), noncoding RNAs (ncRNAs), and undercharacterized modifications (not discussed here) such as chromatin modifications, chromatin accessibility, histone (H) variants (e.g., H3.3, H2A.X, H2A.Z), and RNA modifications (e.g., N6-methyladenosine (m6A)) [296, 364, 367, 391, 393, 399, 402]. Many epigenetic modifications involve covalent bond modifications; however, the main noncovalent epigenetic mechanisms include incorporation of histone variants, nucleosome remodeling, and noncoding RNAs [369]. Chromatin structure and gene expression are regulated by specific amino acids of histone protein tails (consisting of 15–38 amino acids) that undergo various PTMs [366]. Due to the complex diversity among PTMs, the following are considered types of acylation: acetylation, propionylation, butyrylation, crotonylation, 2-hydroxy isobutyrylation, malonylation, succinylation, and glutarylation [403]. Ubiquitylation, sumoylation of lysine residues, and phosphorylation of serine (S) and threonine (T) residues, as well as formylation, O-GlcNAcylation, propionylation, adenosine diphosphate (ADP)-ribosylation, deamination, proline/aspartic acid isomerization, citrullination/eamination, biotinylation, and crotonylation, are reported histone modifications (>200 known modifications) that occur at more than 60 amino acid residues [296, 364, 386, 387, 394, 395].
Epigenetics in Sperm, Epigenetic Diagnostics, and Transgenerational Inheritance
Published in Carlos Simón, Carmen Rubio, Handbook of Genetic Diagnostic Technologies in Reproductive Medicine, 2022
Jennifer L. M. Thorson, Millissia Ben Maamar, Michael K. Skinner
Chemical modifications of RNAs can have dynamic regulatory roles similar to the epigenetic modifications of DNA and histone proteins (41) (Figure 7.1). The most prevalent known mammalian RNA modification is N6-methyladenosine (m6A), a reversible methylation of the messenger RNA (mRNA) (42). The methylation of RNA alters the structure of the RNA to change function and protein or DNA association. Methylation of numerous RNA species results in a diversity of functions on RNA including biophysical, biochemical, and metabolic stabilization of RNA and further crucial functional processes (43).
Identification of m6A-associated LncRNAs as predict factors for the immune infiltration and prognosis of thyroid cancer
Published in Annals of Medicine, 2023
Yongcheng Su, Beibei Xu, Jiangquan Li, Qianwen Shen, Ziyu Lei, Miaomiao Ma, Fuxing Zhang, Tianhui Hu
N6‐methyladenosine (m6A) modification is a type of eukaryotic RNA modification [18] that has been shown to play a regulatory role in numerous human diseases, especially in cancer initiation and progression [19], such as in lung [20], endometrial [21] and liver cancers [22]. It is reported that the upregulation of the m6A regulatory gene METTL14 contributes to pancreatic cancer metastasis [23]. LNCAROD can promote cancer progression through m6A methylation mediated by METTL3 and METTL14 in patients with head and neck squamous cell carcinoma [24]. Similarly, METTL3, a vital m6A methyltransferase, regulates the m6A modification of LINC00958 and affects the prognosis of patients with liver cancer [25]. In addition, recent studies have also shown that the m6A modification is related to immunoregulation [18, 26–29]. However, the underlying mechanism of how m6A-associated lncRNAs are involved in tumour regulation through immune infiltration in THCA remains unclear.
Molecular mechanism analysis of m6A modification-related lncRNA-miRNA-mRNA network in regulating autophagy in acute pancreatitis
Published in Islets, 2022
Xiang Li, Hong Qin, Ali Anwar, Xingwen Zhang, Fang Yu, Zheng Tan, Zhanhong Tang
Recently, the new field of “RNA epigenetics” has been booming, and N6-methyladenosine (m6A) has been identified as a posttranscriptional regulatory mark in multiple RNA species.37 The evidence showed that abnormal m6A methylation plays a significant role in the process of numerous diseases,38–40 and m6A modification of circRNAs may be involved in the pathogenesis of severe AP.19 Therefore, we speculate that m6A modification of lncRNA may also play a role in the AP progression. This study proposed for the first time that m6A modification in AP may mediate the upregulation of lncRNA Pvt1 expression and the downregulation of lncRNA Meg3 and lncRNA AW112010 expression. Consistent with the above, other studies have also found that m6A modification of lncRNA Pvt1 governs epidermal stemness,41 and ALKBH5-mediated m6A modification of lncRNA Pvt1 plays an oncogenic role in osteosarcoma.42 In addition, m6A-induced lncRNA Meg3 suppresses hepatocellular carcinoma cell’s proliferation, migration, and invasion.43 However, no studies have shown that m6A modification of lncRNA AW112010 plays a role in the pathological process, which is the direction we can continue to explore.
Exosome-transmitted circVMP1 facilitates the progression and cisplatin resistance of non-small cell lung cancer by targeting miR-524-5p-METTL3/SOX2 axis
Published in Drug Delivery, 2022
Hongya Xie, Jie Yao, Yuxuan Wang, Bin Ni
N6-methyladenosine (m6A) is the most common post-transcriptional modification in mRNA, which controls the fate of mRNA by regulating various metabolic processes such as mRNA splicing, translation, and degradation (Fustin et al., 2013; Lin et al., 2016). METTL3 is a key member of the m6A methyltransferase complex, and is also a pivotal oncogene for tumor development in multiple malignancies (Zhang et al., 2017; Chen et al., 2018; Weng et al., 2018). SOX2 is a key transcription factor that maintains stem cell characteristics and endows drug resistance (Chaudhary et al., 2019; Mamun et al., 2020). SOX2 is identified as a downstream target of METTL3, and METTL3 is reported to maintain the expression of SOX2 by facilitating its methylation, thereby leading to the progression of glioma (Visvanathan et al., 2018) and colorectal cancer (Li et al., 2019). Here, METTL3 and SOX2 expression was increased in DDP-resistant NSCLC cells. Furthermore, the m6A modification level of SOX2 was also elevated in DD-resistant NSCLC cells. After transfecting with sh-METTL3, the protein level of METTL3 was reduced, and the m6A modification level of SOX2 was decreased, resulting in the degradation of SOX2 mRNA and the down-regulation of SOX2 protein level. We further observed that circVMP1 absence reduced the protein levels of METTL3 and SOX2 and the m6A modification level of SOX2 in NSCLC cells.