Figure - available from: Frontiers in Oncology
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Conjoint analysis of MeRIP-seq and RNA-seq data. (A) Volcano plots showing the differentially expressed genes in tumor vs normal. (B) Heatmap plots showing the differentially expressed genes in tumor vs normal. (C) Four-quadrant plots showing the distribution of genes with significant changes in both the m6A modification and RNA levels. (D) The top 10 GO terms of genes with significant changes in both the m6A modification and mRNA levels. (E) The top 10 KEGG pathways of genes with significant changes in both the m6A modification and RNA levels. (F, G, H, I) GSEA enrichment of genes with significant changes in both the m6A modification and RNA levels.
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N6-methyladenosine (m6A) is the most abundant internal modification on eukaryotic mRNAs. There is increasing evidence that m6A plays a key role in tumor progression, so it is important to analyze m6A modifications within the transcriptome-wide in lung adenocarcinoma (LUAD). Three pairs of LUAD samples and tumor-adjacent normal tissues were obtained...
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Intramuscular fat (IMF) has a pivotal influence on meat quality, with its deposition being a multifaceted physiological interaction of several regulatory factors. N6-methyladenosine (m6A), the preeminent epigenetic alteration among eukaryotic RNA modifications, holds a crucial role in moderating post-transcriptional gene expression. However, there...
Citations
... Thus, ALKBH5 could predict responses to anti-tumor immunotherapy. Methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA sequencing (RNA-seq) identified two genes, Fc receptor-like 5 (FCRL5) and G proteinregulated inducer of neurite outgrowth 1 (GPRIN1), were associated with the prognosis and diagnosis of LUAD patients [171]. YTHDF1 was shown to regulate the expression of FCRL5 and GPRIN1 [171]. ...
... Methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA sequencing (RNA-seq) identified two genes, Fc receptor-like 5 (FCRL5) and G proteinregulated inducer of neurite outgrowth 1 (GPRIN1), were associated with the prognosis and diagnosis of LUAD patients [171]. YTHDF1 was shown to regulate the expression of FCRL5 and GPRIN1 [171]. Genes with dysregulated m6A modifications were enriched in cancer signaling pathways [171]. ...
... YTHDF1 was shown to regulate the expression of FCRL5 and GPRIN1 [171]. Genes with dysregulated m6A modifications were enriched in cancer signaling pathways [171]. Transcriptomic and m6A methylomic studies showed that adenocarcinoma of the esophagogastric junction (AEG) was correlated with the dysregulation of m6A RNA modifications [172]. ...
RNA methylations play critical roles in RNA processes, including RNA splicing, nuclear export, nonsense-mediated RNA decay, and translation. Regulators of RNA methylations have been shown to be differentially expressed between tumor tissues/cancer cells and adjacent tissues/normal cells. N6-methyladenosine (m6A) is the most prevalent internal modification of RNAs in eukaryotes. m6A regulators include m6A writers, m6A demethylases, and m6A binding proteins. Since m6A regulators play important roles in regulating the expression of oncogenes and tumor suppressor genes, targeting m6A regulators can be a strategy for developing anticancer drugs. Anticancer drugs targeting m6A regulators are in clinical trials. m6A regulator-targeting drugs could enhance the anticancer effects of current chemotherapy drugs. This review summarizes the roles of m6A regulators in cancer initiation and progression, autophagy, and anticancer drug resistance. The review also discusses the relationship between autophagy and anticancer drug resistance, the effect of high levels of m6A on autophagy and the potential values of m6A regulators as diagnostic markers and anticancer therapeutic targets.
Cellular senescence is a state of irreversible cellular growth arrest that occurs in response to various stresses. In addition to exiting the cell cycle, senescent cells undergo many phenotypic alterations, including metabolic reprogramming, chromatin rearrangement, and senescence-associated secretory phenotype (SASP) development. Furthermore, senescent cells can affect most physiological and pathological processes, such as physiological development; tissue homeostasis; tumour regression; and age-associated disease progression, including diabetes, atherosclerosis, Alzheimer's disease, and hypertension. Although corresponding anti-senescence therapies are actively being explored for the treatment of age-associated diseases, the specific regulatory mechanisms of senescence remain unclear. N 6-methyladenosine (m 6A), a chemical modification commonly distributed in eukaryotic RNA, plays an important role in biological processes such as translation, shearing, and RNA transcription. Numerous studies have shown that m 6A plays an important regulatory role in cellular senescence and aging-related disease. In this review, we systematically summarize the role of m 6A modifications in cellular senescence with regard to oxidative stress, DNA damage, telomere alterations, and SASP development. Additionally, diabetes, atherosclerosis, and Alzheimer's disease regulation via m 6A-mediated cellular senescence is discussed. We further discuss the challenges and prospects of m 6A in cellular senescence and age-associated diseases with the aim of providing rational strategies for the treatment of these age-associated diseases.
