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Title:
Writers, readers, and erasers RNA modifications and drug resistance in cancer | Molecular Cancer
Description:
Drug resistance in cancer cells significantly diminishes treatment efficacy, leading to recurrence and metastasis. A critical factor contributing to this resistance is the epigenetic alteration of gene expression via RNA modifications, such as N6-methyladenosine (m6A), N1-methyladenosine (m1A), 5-methylcytosine (m5C), 7-methylguanosine (m7G), pseudouridine (Ψ), and adenosine-to-inosine (A-to-I) editing. These modifications are pivotal in regulating RNA splicing, translation, transport, degradation, and stability. Governed by “writers,” “readers,” and “erasers,” RNA modifications impact numerous biological processes and cancer progression, including cell proliferation, stemness, autophagy, invasion, and apoptosis. Aberrant RNA modifications can lead to drug resistance and adverse outcomes in various cancers. Thus, targeting RNA modification regulators offers a promising strategy for overcoming drug resistance and enhancing treatment efficacy. This review consolidates recent research on the role of prevalent RNA modifications in cancer drug resistance, with a focus on m6A, m1A, m5C, m7G, Ψ, and A-to-I editing. Additionally, it examines the regulatory mechanisms of RNA modifications linked to drug resistance in cancer and underscores the existing limitations in this field.
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Keywords {🔍}
pubmed, article, google, scholar, cancer, cas, rna, resistance, central, cell, modifications, modification, wang, cells, drug, zhang, httpsdoiorgs, chen, mettl, mrna, liu, methylation, tumor, expression, mol, targeting, therapeutic, nmethyladenosine, editing, res, immune, promotes, role, rnas, protein, yang, nat, rev, sci, biol, signaling, huang, cancers, enhances, enhancing, dna, alkbh, zhao, therapy, fto,
Topics {✒️}
n6–methyladenosine upregulates mir–181d–5p exosomal mir-181d-5p derived tki targeting c-met/alk/ros1 hsa-linc02418/mmu-4930573i07rik regulated regulating mir-149-3p/s100a4/p53 axis raf/mek/erk signaling pathway crispr-cas-mediated genome editing trmt6/61a-dependent base methylation trim21-mediated pd-l1 ubiquitination y-box-binding protein ybx1 azgp1p2/uba1/rbm15 cascade mediates accelerating pri-microrna-221-3p maturation crispr/cas9-based epigenome editing anti-pd-l1 antibody atezolizumab m6a-mediated pd-1/pd-l1 linc00942–msi2–c-myc axis disrupt rig-i-mediated activation n6-adenosine-methyltransferase subunits mettl3 wnt/β-catenin signaling pathway pi3k/akt/mtor signaling pathway azgp1p2/uba1/rbm15/tpm1 cascade activating wnt/β-catenin pathway article download pdf cap-binding protein eif4e hsf4b/hsp90b1/mutant p53 axis aly/ref export factor azgp1p2/uba1/rbm15/tpm1 pathway promotes mir-146a expression crispr/cas enzymes suggests high c-met expression increased mir-221-3p expression plga-based nanoplatform loaded induce epithelial-mesenchymal transition lncrna-mediated posttranslational modifications synergistic chemo-photothermal therapy demethylase alkbh5-mediated upregulation castration-sensitive prostate cancer reduced ck2α-mediated glycolysis mettl1/wdr4-mediated trna mir-570-3p/spp1 axis intrinsic pro-tumorigenic genes post-transcriptionally regulating key elevated snhg17 facilitates n6-methyladenosine rna modification rna n6-methyladenosine modification rna modification n6-methyladenosine targeting epithelial-mesenchymal transition distinct n7-methylguanosine profiles proline-rich coiled-coil n6 methyladenosine-dependent mechanism
Questions {❓}
- How the Warburg effect supports aggressiveness and drug resistance of cancer cells?
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headline:Writers, readers, and erasers RNA modifications and drug resistance in cancer
description:Drug resistance in cancer cells significantly diminishes treatment efficacy, leading to recurrence and metastasis. A critical factor contributing to this resistance is the epigenetic alteration of gene expression via RNA modifications, such as N6-methyladenosine (m6A), N1-methyladenosine (m1A), 5-methylcytosine (m5C), 7-methylguanosine (m7G), pseudouridine (Ψ), and adenosine-to-inosine (A-to-I) editing. These modifications are pivotal in regulating RNA splicing, translation, transport, degradation, and stability. Governed by “writers,” “readers,” and “erasers,” RNA modifications impact numerous biological processes and cancer progression, including cell proliferation, stemness, autophagy, invasion, and apoptosis. Aberrant RNA modifications can lead to drug resistance and adverse outcomes in various cancers. Thus, targeting RNA modification regulators offers a promising strategy for overcoming drug resistance and enhancing treatment efficacy. This review consolidates recent research on the role of prevalent RNA modifications in cancer drug resistance, with a focus on m6A, m1A, m5C, m7G, Ψ, and A-to-I editing. Additionally, it examines the regulatory mechanisms of RNA modifications linked to drug resistance in cancer and underscores the existing limitations in this field.
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Epigenetic alterations
Drug resistance
Abnormal expression
Combination therapy
RNA modification regulators
Cancer Research
Oncology
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description:Drug resistance in cancer cells significantly diminishes treatment efficacy, leading to recurrence and metastasis. A critical factor contributing to this resistance is the epigenetic alteration of gene expression via RNA modifications, such as N6-methyladenosine (m6A), N1-methyladenosine (m1A), 5-methylcytosine (m5C), 7-methylguanosine (m7G), pseudouridine (Ψ), and adenosine-to-inosine (A-to-I) editing. These modifications are pivotal in regulating RNA splicing, translation, transport, degradation, and stability. Governed by “writers,” “readers,” and “erasers,” RNA modifications impact numerous biological processes and cancer progression, including cell proliferation, stemness, autophagy, invasion, and apoptosis. Aberrant RNA modifications can lead to drug resistance and adverse outcomes in various cancers. Thus, targeting RNA modification regulators offers a promising strategy for overcoming drug resistance and enhancing treatment efficacy. This review consolidates recent research on the role of prevalent RNA modifications in cancer drug resistance, with a focus on m6A, m1A, m5C, m7G, Ψ, and A-to-I editing. Additionally, it examines the regulatory mechanisms of RNA modifications linked to drug resistance in cancer and underscores the existing limitations in this field.
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Drug resistance
Abnormal expression
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RNA modification regulators
Cancer Research
Oncology
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