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Long non-coding RNA radiation induced regulator of PLK1 and RAD51 (lnc-RI)

Target
lnc-RI
Molecular classification
Long non-coding RNA (lncRNA), Epigenetic regulator
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Overview

lnc-RI (Long non-coding RNA radiation induced regulator of PLK1 and RAD51) is a long non-coding RNA identified as a novel regulator of DNA repair by homologous recombination, primarily by stabilizing RAD51 mRNA through competitive binding to microRNA-193a-3p (ceRNA mechanism)[1]. Knockdown of lnc-RI suppresses homologous recombination repair efficiency, depresses the expression of several HR pathway proteins (including RAD51 and PLK1), and leads to increased DNA double-strand breaks and genomic instability. Its regulatory role is most pronounced in cell cycle S/G2 phases and impacts radiation sensitivity and cancer risk. lnc-RI has emerged as a potential biomarker and candidate therapeutic target due to its critical function in DNA repair and maintenance of genomic integrity[1].

Other names
lnc-RILong non-coding RNA radiation induced regulator of PLK1 and RAD51LncRNA radiation induced regulator of PLK1 and RAD51
02

Mechanism of action

Not applicable. No drugs currently specifically target lnc-RI; thus, mechanism of action for drugs is unavailable. Potential mechanism: RNA interference or antisense oligonucleotides could hypothetically downregulate lnc-RI[1].

03

Biological functions

Regulation of homologous recombination repair (HR) of DNA double-strand breaksRegulation of RAD51 mRNA stabilityCell cycle progressionMaintenance of genomic stabilityCompetitive endogenous RNA (ceRNA) activity
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Disease associations

CancerGenomic instability disorders
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Safety considerations

Genomic instability risk if lnc-RI is downregulatedPotential for unwanted DNA damage accumulation or cell cycle arrestOff-target effects in therapeutic applications targeting non-coding RNAs are a general concern.
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Biomarkers

lnc-RI expression levelMicronucleus frequencyPossibly RAD51/PLK1 expression under lnc-RI perturbation, as surrogate markers

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