Related Experiment Video
Updated: Aug 12, 2025
RNA Pull-down Procedure to Identify RNA Targets of a Long Non-coding RNA
Published on: April 10, 2018
Activation of long-non-coding RNA NEAT1 sponging microRNA-147 inhibits radiation damage by targeting PDPK1 in
Yong-Jian Hu1,2, Gui-Yuan Song1,3,4, Fan Zhang1,2
1School of Food and Biomedicine, Zaozhuang University, Zaozhuang, Shandong 277160, China.
Abstract:
A better understanding of the molecular mechanism involving the lncRNA-miRNA-mRNA network underlying radiation damage can be beneficial for radioprotection. This study was designed to investigate the potential role of lncRNA NEAT1, miR-147 and Phosphoinositide Dependent Protein Kinase 1 (PDPK1) interaction in radioprotection by troxerutin (TRT). We first demonstrated that NEAT1 sponged miR-147, and PDPK1 mRNA was the primary target of miR-147. In the cells, the NEAT1 and PDPK1 levels were downregulated after the radiation but increased after the treatment with TRT. The miR-147 level was significantly induced by radiation and inhibited by TRT. NEAT1 negatively regulated the expression of miR-147, whereas miR-47 targeted PDPK1 to downregulate its expression. In radioprotection, TRT effectively upregulated NEAT1 to inhibit miR-147 and to upregulate PDPK1. We concluded that TRT could promote radioprotection by stimulating NEAT1 to upregulate PDPK1 expression by suppressing miR-147. NEAT1 could be a critical therapeutic target of radiation damage.
Insights
Troxerutin (TRT) enhances radioprotection by modulating the NEAT1-miR-147-PDPK1 pathway. TRT upregulates NEAT1, which suppresses miR-147, ultimately increasing PDPK1 expression to protect against radiation damage.
Area of Science:
- Molecular Biology
- Radioprotection Research
- Non-coding RNA Function
Background:
- Understanding the molecular mechanisms of radiation damage is crucial for developing effective radioprotective strategies.
- The lncRNA-miRNA-mRNA regulatory network plays a significant role in cellular responses to radiation.
- Long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1), microRNA-147 (miR-147), and Phosphoinositide Dependent Protein Kinase 1 (PDPK1) are implicated in cellular processes.
Purpose of the Study:
- To investigate the interaction between lncRNA NEAT1, miR-147, and PDPK1 in the context of radioprotection mediated by troxerutin (TRT).
- To elucidate the molecular pathway through which TRT confers protection against radiation-induced damage.
Main Methods:
- Investigated the sponging activity of NEAT1 on miR-147.
- Identified PDPK1 mRNA as a direct target of miR-147.
- Analyzed the expression levels of NEAT1, miR-147, and PDPK1 in cells exposed to radiation and treated with TRT.
- Determined the regulatory relationships between NEAT1, miR-147, and PDPK1.
Main Results:
- NEAT1 was shown to sponge miR-147, and miR-147 directly targeted PDPK1 mRNA.
- Radiation exposure downregulated NEAT1 and PDPK1 but upregulated miR-147.
- TRT treatment reversed these effects, increasing NEAT1 and PDPK1 while decreasing miR-147.
- TRT promoted radioprotection by upregulating NEAT1, which inhibited miR-147, leading to increased PDPK1 expression.
Conclusions:
- TRT confers radioprotection by activating the NEAT1/miR-147/PDPK1 axis.
- NEAT1 acts as a crucial regulator in this pathway, upregulating PDPK1 by suppressing miR-147.
- NEAT1 represents a potential therapeutic target for mitigating radiation damage.
Related Concept Videos
02:39lncRNA - Long Non-coding RNAs
01:38Nucleotide Excision Repair
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...