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Title:
RNA demethylase ALKBH5 in cancer: from mechanisms to therapeutic potential | Journal of Hematology & Oncology
Description:
RNA demethylase ALKBH5 takes part in the modulation of N6-methyladenosine (m6A) modification and controls various cell processes. ALKBH5-mediated m6A demethylation regulates gene expression by affecting multiple events in RNA metabolism, e.g., pre-mRNA processing, mRNA decay and translation. Mounting evidence shows that ALKBH5 plays critical roles in a variety of human malignancies, mostly via post-transcriptional regulation of oncogenes or tumor suppressors in an m6A-dependent manner. Meanwhile, increasing non-coding RNAs are recognized as functional targets of ALKBH5 in cancers. Here we reviewed up-to-date findings about the pathological roles of ALKBH5 in cancer, the molecular mechanisms by which it exerts its functions, as well as the underlying mechanism of its dysregulation. We also discussed the therapeutic implications of targeting ALKBH5 in cancer and potential ALKBH5-targeting strategies.
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Keywords {๐}
alkbh, pubmed, cancer, article, google, scholar, cas, cell, central, rna, cells, expression, mrna, wang, tumor, demethylase, cancers, targeting, promotes, zhang, protein, demethylation, modification, methylation, binding, stem, liu, nmethyladenosine, human, gene, regulation, carcinoma, rnas, fig, target, chen, yang, functions, histone, res, role, regulates, breast, immune, nsclc, proliferation, therapeutic, potential, roles, dna,
Topics {โ๏ธ}
activating atm-chk2-p53/cdc25c signaling pre-mir-181b-1/yap signaling axis naturally-derived small-molecule inhibitors kdm4c-alkbh5-axl signaling axis mir-193a-3p promotes growth mir-193a-3p transfection results mrna-binding factor rbm15/spenito suppresses mir-193a-3p maturation oxygenase double-stranded ฮฒ-helix programmable m6a-editing systems comprises argโser-rich regions cell-type-specific methylation patterns myb proto-oncogene c-myb dead-box rna helicase n6-methyladenosine rna demethylase n6-methyladenosine-modified rna article download pdf alkbh5-mediated post-transcriptional regulation controls sorafenib-induced autophagy mirna-193a-3p regulates rna n6-methyladenosine methyltransferase m6a-dependent epigenetic silencing transcriptional pre-mrna splicing circular rna-protein interactions full-length human alkbh5 primary mir-193a-3p alkbh5 post-transcriptionally regulates m6a-ck2alpha-mediated glycolysis m6a-ythdf2-dependent fashion crisprโcas13b-based tool m6a-guided epigenetic inhibition hypoxia-inducible factor 1alpha n6-methyladenosine alkbh5 promotes ctcf ccctc-binding factor n6-methyladenosine-dependent regulation crispr-based m6a targeting n6-methyladenosine binding protein post-transcriptionally regulating tacc3 n6-methyladenosine-independent manner single-nucleotide-resolution mapping small-molecule inhibitors targeting circrnas represent single-stranded double-stranded nucleic acids crispr-based gene therapy m6a-ythdf2-dependent manner mixed-lineage leukemia protein n6-methyladenosine binding induces arrows represent ฮฒ-strands alkbh5-mediated m6a demethylation alkbh5-mediated m6a-demethylation
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headline:RNA demethylase ALKBH5 in cancer: from mechanisms to therapeutic potential
description:RNA demethylase ALKBH5 takes part in the modulation of N6-methyladenosine (m6A) modification and controls various cell processes. ALKBH5-mediated m6A demethylation regulates gene expression by affecting multiple events in RNA metabolism, e.g., pre-mRNA processing, mRNA decay and translation. Mounting evidence shows that ALKBH5 plays critical roles in a variety of human malignancies, mostly via post-transcriptional regulation of oncogenes or tumor suppressors in an m6A-dependent manner. Meanwhile, increasing non-coding RNAs are recognized as functional targets of ALKBH5 in cancers. Here we reviewed up-to-date findings about the pathological roles of ALKBH5 in cancer, the molecular mechanisms by which it exerts its functions, as well as the underlying mechanism of its dysregulation. We also discussed the therapeutic implications of targeting ALKBH5 in cancer and potential ALKBH5-targeting strategies.
datePublished:2022-01-21T00:00:00Z
dateModified:2022-01-21T00:00:00Z
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license:http://creativecommons.org/publicdomain/zero/1.0/
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keywords:
m6A modification
ALKBH5
RNA demethylation
Cancer
Gene regulation
Therapeutic target
Oncology
Hematology
Cancer Research
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headline:RNA demethylase ALKBH5 in cancer: from mechanisms to therapeutic potential
description:RNA demethylase ALKBH5 takes part in the modulation of N6-methyladenosine (m6A) modification and controls various cell processes. ALKBH5-mediated m6A demethylation regulates gene expression by affecting multiple events in RNA metabolism, e.g., pre-mRNA processing, mRNA decay and translation. Mounting evidence shows that ALKBH5 plays critical roles in a variety of human malignancies, mostly via post-transcriptional regulation of oncogenes or tumor suppressors in an m6A-dependent manner. Meanwhile, increasing non-coding RNAs are recognized as functional targets of ALKBH5 in cancers. Here we reviewed up-to-date findings about the pathological roles of ALKBH5 in cancer, the molecular mechanisms by which it exerts its functions, as well as the underlying mechanism of its dysregulation. We also discussed the therapeutic implications of targeting ALKBH5 in cancer and potential ALKBH5-targeting strategies.
datePublished:2022-01-21T00:00:00Z
dateModified:2022-01-21T00:00:00Z
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m6A modification
ALKBH5
RNA demethylation
Cancer
Gene regulation
Therapeutic target
Oncology
Hematology
Cancer Research
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Libraries {๐}
- Clipboard.js
- Prism.js
CDN Services {๐ฆ}
- Crossref