ArticleMolecular therapy. Nucleic acids2022
Double-stranded RNA induction asa potential dynamic biomarkerfor DNA-demethylating agents.
Article in Molecular therapy. Nucleic acids, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- LPAR4 mediates resistance to interferon-induced stress in soft tissue sarcoma.Science advances · 2026Article
- Deciphering the multifaceted role of double-stranded RNA sensor protein kinase R: pathophysiological function beyond the antiviral response.RNA biology · 2025Review
- Toward unraveling molecular grammars for dsRNA-binding proteins: substrate recognition to binding mechanisms.BMB reports · 2025Review
- Comparative outcome and prognostic factor analysis among MDS/AML patients with TP53 mutations, snps, and wild type.Human genomics · 2025Article
- SLIRP amplifies antiviral signaling via positive feedback regulation and contributes to autoimmune diseases.Cell reports · 2025Article
- Cellular dsRNA interactome captured by K1 antibody reveals the regulatory map of exogenous RNA sensing.Communications biology · 2025Article
- Targeting mitochondrial RNAs enhances the efficacy of the DNA-demethylating agents.Scientific reports · 2024Article
- Double-Stranded RNA-Based Method for Diagnosing Severe Fever with Thrombocytopenia.Journal of clinical medicine · 2024Article
- The Versatile Roles of nc886, a Fascinating and Peculiar Regulatory Non-Coding RNA, in Cancer.International journal of molecular sciences · 2024Review
- Inverted Alu repeats: friends or foes in the human transcriptome.Experimental & molecular medicine · 2024Review
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Authors and funding
15 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Hypomethylating agents (HMAs), such as azacitidine and decitabine, induce cancer cell death by demethylating DNAs to promote the expression of tumor-suppressor genes. HMAs also reactivate the transcription of endogenous double-stranded RNAs (dsRNAs) that trigger the innate immune response and subsequent apoptosis via viral mimicry. However, the expression patterns of endogenous dsRNAs and their relevance in the efficacy of HMAs remain largely uninvestigated. Here, we employ amidine-conjugated spiropyran (Am-SP) to examine the dynamic expression pattern of total dsRNAs regulated by HMAs. By analyzing the bone-marrow aspirates of myelodysplastic syndrome or acute myeloid leukemia patients who received the HMAs, we find a dramatic increase in total dsRNA levels upon treatment only in patients who later benefited from the therapy. We further apply our approach in solid tumor cell lines and show that the degree of dsRNA induction correlates with the effectiveness of decitabine in most cases. Notably, when dsRNA induction is accompanied by increased expression of nc886 RNA, decitabine becomes ineffective. Collectively, our study establishes the potential application of monitoring the total dsRNA levels by a small molecule as an analytical method and a dynamic marker to predict the clinical outcome of the HMA therapy.
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