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We began analyzing https://www.nature.com/articles/s41419-017-0129-x, but it redirected us to https://www.nature.com/articles/s41419-017-0129-x. The analysis below is for the second page.

Title[redir]:
N6-methyladenosine links RNA metabolism to cancer progression | Cell Death & Disease
Description:
N6-methyladenosine (m6A) is the most abundant mRNA modification. With the development of antibody-based sequencing technologies and the findings of m6A-related “writers”, “erasers”, and “readers”, the relationships between m6A and mRNA metabolism are emerging. The m6A modification influences almost every step of RNA metabolism that comprises mRNA processing, mRNA exporting from nucleus to cytoplasm, mRNA translation, mRNA decay, and the biogenesis of long-non-coding RNA (lncRNA) and microRNA (miRNA). Recently, more and more studies have found m6A is associated with cancer, contributing to the self-renewal of cancer stem cell, promotion of cancer cell proliferation, and resistance to radiotherapy or chemotherapy. Inhibitors of m6A-related factors have been explored, and some of them were identified to inhibit cancer progression, indicating that m6A could be a target for cancer therapy. In this review, we are trying to summarize the regulation and function of m6A in human carcinogenesis.

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Science
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Keywords {🔍}

pubmed, article, google, scholar, cas, mettl, cancer, rna, cell, mrna, fto, cells, central, alkbh, found, nature, metabolism, translation, stem, protein, ythdf, splicing, nmethyladenosine, level, processing, overexpression, expression, modification, knockdown, complex, nuclear, site, regulation, human, methylation, progression, factors, mirna, rnas, sites, mrnas, tumor, increased, breast, growth, biol, role, mata, damage, chem,

Topics {✒️}

nature portfolio privacy policy advertising lncrna x-inactive-specific transcript social media isogenic idh2-wt-expressing cells reprints al single-nucleotide-resolution mapping n6-methyladenosine rna demethylase open questions antibody-based sequencing technologies nadp+-dependent oxidative decarboxylation n6-methyladenosine-modified rna chemicals targeting n6-methyladenosine mir-33a suppresses proliferation early uv-induced damage rna n6-methyladenosine methyltransferase n6-methyladenosine-dependent regulation mrna n6-adenosine methyltransferase arta-induced drug response promotes cap-independent translation rna n6-methyladenosine modifications mir-145-5p inhibits proliferation nature 543 nature 537 nature 518 nature 505 nature 485 nature 519 nature 464 nature 488 nature pre-mrna indirectly alters /alpha-ketoglutarate-dependent dioxygenases promote cap-independent translation39 α-ketoglutarate-dependent dioxygenases idh1/2-wt aml cells fto-overexpressing aml cells hypo-methylated m6a peaks human hydroxyacid-oxoacid transhydrogenase data shed lights small-cell lung cancer uv-treated u2os cells uv laser micro-irradiation original author single-stranded rna acute myeloid leukemia intron-specific region subsequent drug development nuclear member ythdc1

Questions {❓}

Are snoRNAs and snoRNA host genes new players in cancer?
Are there more “writers”, “erasers”, and “readers” in the regulation of N6-methyladenosine?
Could N6-methyladenosine be an effective target for cancer therapy?
What is the potential connection of other RNA modifications with N6-methyladenosine?

Schema {🗺️}

WebPage:
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