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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].
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].
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