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Keywords {🔍}

pubmed, article, google, scholar, cas, central, cancer, cell, wang, ferroptosis, zhang, chen, liu, rna, wei, carcinoma, yang, modification, cells, methylation, mettl, promotes, nmethyladenosine, res, mol, progression, shi, death, zhou, biol, tang, mrna, nat, zheng, huang, sci, zhao, regulates, jiang, guo, fto, lung, med, demethylase, hepatocellular, metabolism, gao, alkbh, sun, china,

Topics {✒️}

n6-methyladenosine-dependent post-transcriptional modification thiol-based sensor-effector apparatus controlling n6-methyladenosine-based epitranscriptomics promoting otub1-mediated anti-ferroptosis kcnq1ot1-mir-7-5p-tfrc axis p62-keap1-nrf2 pathway protects month download article/chapter mrna n6-adenosine methyltransferase m6 a-igf2bp2-dependent manner n6-methyladenosine-modified rna rna n6-methyladenosine methyltransferase colistin-induced kidney injury inhibit erastin-induced ferroptosis ythdf1-mediated m6a modification preventing m6a-mediated degradation tiam1-nrf2/ho-1 axis n6-methyladenosine fto demethylase targeting β-catenin wtap-mediated m6a modification ferroptosis-related lncrna signature wtap-wt1-tbl1 axis n6-methyladenosine modification involved mettl3-eif3h enhances translation posttranscriptionally activating nfe2l2/nrf2 m6a-ythdf2-dependent modulation wei xiong & ming zhou modulating m6a-modified scd1 s-adenosyl homocysteine hydrolase accelerating pri-mir221/222 maturation single-nucleotide-resolution mapping reversing egfr-tkis resistance methyl-specific binding proteins essential n6-methyladenosine biotarget iron-dependent cell death enhancing c-myc stability p53-mediated tumour suppression glutathione-bioimprinted nanoparticles targeting m6a-dependent ferroptosis regulation platinum-based cancer therapy m6a-related ferroptosis signature m6a reader ythdc2 targets pre-mrnas targeting m6a/ferroptosis pathway modulating keap1/nrf2 pathway multiple redox-active enzymes wnt signalling pathway glutathione-independent ferroptosis suppressor tfrc m6a methylation mediating wnt signaling central south university

Questions {❓}

• The role of SLC7A11 in cancer: friend or foe?

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         headline:Ferroptosis: a critical mechanism of N6-methyladenosine modification involved in carcinogenesis and tumor progression
         description:Ferroptosis is an iron-dependent regulatory cell necrosis induced by iron overload and lipid peroxidation. It occurs when multiple redox-active enzymes are ectopically expressed or show abnormal function. Hence, the precise regulation of ferroptosis-related molecules is mediated across multiple levels, including transcriptional, posttranscriptional, translational, and epigenetic levels. N6-methyladenosine (m6A) is a highly evolutionarily conserved epigenetic modification in mammals. The m6A modification is commonly linked to tumor proliferation, progression, and therapy resistance because it is involved in RNA metabolic processes. Intriguingly, accumulating evidence suggests that dysregulated ferroptosis caused by the m6A modification drives tumor development. In this review, we summarized the roles of m6A regulators in ferroptosis-mediated malignant tumor progression and outlined the m6A regulatory mechanism involved in ferroptosis pathways. We also analyzed the potential value and application strategies of targeting m6A/ferroptosis pathway in the clinical diagnosis and therapy of tumors.
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      headline:Ferroptosis: a critical mechanism of N6-methyladenosine modification involved in carcinogenesis and tumor progression
      description:Ferroptosis is an iron-dependent regulatory cell necrosis induced by iron overload and lipid peroxidation. It occurs when multiple redox-active enzymes are ectopically expressed or show abnormal function. Hence, the precise regulation of ferroptosis-related molecules is mediated across multiple levels, including transcriptional, posttranscriptional, translational, and epigenetic levels. N6-methyladenosine (m6A) is a highly evolutionarily conserved epigenetic modification in mammals. The m6A modification is commonly linked to tumor proliferation, progression, and therapy resistance because it is involved in RNA metabolic processes. Intriguingly, accumulating evidence suggests that dysregulated ferroptosis caused by the m6A modification drives tumor development. In this review, we summarized the roles of m6A regulators in ferroptosis-mediated malignant tumor progression and outlined the m6A regulatory mechanism involved in ferroptosis pathways. We also analyzed the potential value and application strategies of targeting m6A/ferroptosis pathway in the clinical diagnosis and therapy of tumors.
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