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Updated: May 19, 2026
Sequence-specific and Selective Recognition of Double-stranded RNAs over Single-stranded RNAs by Chemically Modified Peptide Nucleic Acids
Published on: September 21, 2017
RNA duplex formation and competing endogenous RNA, proposed as mechanisms in regulating expression of natural
Richi Nakatake1, Tetsuya Okuyama1, Tominori Kimura2
1Department of Pancreatobiliary Surgery, Kansai Medical University, Hirakata, Osaka, Japan.
Abstract:
Natural antisense transcripts (NATs) from eukaryotic genes, known as long non-coding RNAs (lncRNAs), are long transcripts that do not encode proteins. NATs play diverse functional roles in regulating the transcription, stability, and translation of protein-coding genes at the epigenetic and post-transcriptional levels. Here, we outline recent studies on NAT-mediated RNA networks and discuss their potential as therapeutic targets across diseases. Interferon-α1 (IFNA1) mRNA expression is regulated by its overlapping antisense transcript IFNA1-AS through IFNA1 mRNA-AS duplex formation, and microRNA-sponging through common microRNA response elements (MREs) as competing endogenous RNAs. The competitive interactions between NATs and mRNA MRE(s) fine-tune mRNA and protein levels. The receptor tyrosine kinase, ephrin type-A receptor 2 (EPHA2) mRNA and its antisense partner (EPHA2-AS) are transcribed from the EPHA2 gene and are overexpressed in breast cancer. EPHA2-AS interacts with EPHA2 mRNA, forming an mRNA-AS duplex that modulates both EPHA2 mRNA and protein levels, potentially contributing to tumorigenesis; hence, it is a potential target for breast cancer treatment. RNA methylation, such as N 6-methyladenosine, may also play a role in regulating gene expression in various diseases. NAT-targeted therapeutics, such as synthetic oligonucleotides, mRNA, and drugs, can be introduced into cells either directly or via extracellular vesicles and lipid nanoparticles. The administration of NAT-targeted therapeutics in animal disease models is useful for evaluating their efficacy. The mechanisms of NAT-mediated gene regulation should be further investigated to develop NAT-targeted therapeutics for the treatment of various diseases.
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