Abstract
Dicer-deficient cancers have poor prognoses, which is linked to the degradation of tumour-suppressing miRNA precursors by the Translin-Trax (Tn-Tx) ribonuclease. Inhibition of Tn-Tx potentially offers a new therapeutic intervention point. However, Tn-Tx functions in an array of biological processes, and here we consider how this complexity could influence therapeutic design strategies.
Keywords:
DNA repair; Dicer; Translin-Trax; drug development; miRNA.
Copyright © 2020 Elsevier Inc. All rights reserved.
MeSH terms
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Antineoplastic Agents / pharmacology*
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Antineoplastic Agents / therapeutic use
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Carcinogenesis / drug effects
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Carcinogenesis / genetics
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DEAD-box RNA Helicases / metabolism
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DNA Breaks, Double-Stranded
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DNA End-Joining Repair / drug effects
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DNA-Binding Proteins / antagonists & inhibitors*
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DNA-Binding Proteins / metabolism
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Drug Design
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Gene Expression Regulation, Neoplastic / drug effects
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Genes, Tumor Suppressor
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Humans
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MicroRNAs / metabolism
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Molecular Targeted Therapy / methods
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Neoplasms / drug therapy*
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Neoplasms / genetics
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RNA Precursors / metabolism*
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RNA Stability / drug effects
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Ribonuclease III / metabolism
Substances
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Antineoplastic Agents
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DNA-Binding Proteins
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MicroRNAs
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RNA Precursors
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TSN protein, human
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TSNAX protein, human
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DICER1 protein, human
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Ribonuclease III
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DEAD-box RNA Helicases