Related Experiment Video
Updated: Jun 25, 2025
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Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
Published on: November 19, 2019
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LncRNA AP000842.3 Triggers the Malignant Progression of Prostate Cancer by Regulating Cuproptosis Related Gene NFAT5
Gaobo Zhou1, Chaoqian Chen1, Hongjian Wu1
1Department of Urology, Taizhou Hospital of Zhejiang Province affiliated to Wenzhou Medical University, Taizhou, China.
Technology in Cancer Research & Treatment
|May 23, 2024
Summary
This study reveals a novel ceRNA network involving lncRNA AP000842.3, miR-206, and NFAT5 in prostate cancer (PRAD). This network regulates cuproptosis sensitivity and PRAD progression, offering potential diagnostic and therapeutic targets.
Area of Science:
- Oncology
- Molecular Biology
- Cell Death Research
Background:
- Prostate cancer (PRAD) is a major malignancy with complex genetic regulation.
- Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) play key roles in PRAD via competing endogenous RNA (ceRNA) networks.
- Cuproptosis, a novel cell death pathway, and Nuclear factor of activated T cells 5 (NFAT5) are implicated in tumor development, but their interplay in PRAD's ceRNA network is unknown.
Purpose of the Study:
- To elucidate the regulatory mechanism of NFAT5 within the ceRNA network in prostate cancer.
- To investigate the role of the lncRNA AP000842.3/miR-206/NFAT5 axis in PRAD progression and cuproptosis.
- To identify potential diagnostic and therapeutic targets for PRAD based on ceRNA network interactions.
Main Methods:
- Bioinformatics analysis to identify the ceRNA axis regulating cuproptosis.
- Reactive oxygen species (ROS) and copper ion concentration assays to assess cuproptosis sensitivity.
- Luciferase reporter assays to confirm the interaction between AP000842.3, miR-206, and NFAT5.
Main Results:
- lncRNA AP000842.3 functions as a ceRNA for miR-206, thereby regulating NFAT5 expression in PRAD.
- Inhibition of NFAT5 enhances PRAD sensitivity to cuproptosis inducers.
- Alterations in AP000842.3 and miR-206 expression impact PRAD proliferation by modulating NFAT5 levels, with partial dependence on miR-206.
Conclusions:
- A crucial ceRNA regulatory network (AP000842.3/miR-206/NFAT5) is identified in prostate cancer.
- This network influences PRAD progression and cuproptosis, highlighting NFAT5 as a key regulator.
- The discovered ceRNA network presents a promising avenue for novel diagnostic and therapeutic strategies in PRAD.
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