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Identification of RNAs Engaged in Direct RNA-RNA Interaction with a Long Non-Coding RNA
Published on: July 9, 2021
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Targeting LncRNA ADAMTS9-AS1 is a Promising Therapeutic Strategy to Inhibit the Progression of Bladder Cancer
Zhu Yu1, Gongxiang Tan1, Chunyan Yu1
1Department of Urology, The 908th Hospital of Joint Logistic Support Force of PLA, 330000 Nanchang, Jiangxi, China.
Discovery Medicine
|December 27, 2024
Summary
This study reveals that ADAMTS9-AS1, a long non-coding RNA, is decreased in bladder cancer (BC). Restoring ADAMTS9-AS1 levels enhances cisplatin sensitivity by targeting FUS, offering a potential therapeutic strategy for BC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Bladder cancer (BC) is a prevalent malignancy with aggressive characteristics.
- Improving cisplatin sensitivity is crucial for effective BC treatment.
- Identifying novel molecular targets is essential for therapeutic advancements.
Purpose of the Study:
- To investigate the expression of long non-coding RNA (lncRNA) ADAMTS9-AS1 in BC.
- To explore the mechanism by which ADAMTS9-AS1 influences cisplatin sensitivity.
- To evaluate ADAMTS9-AS1 as a potential therapeutic target for BC.
Main Methods:
- Retrospective analysis of BC tissues and adjacent normal tissues from 10 patients.
- In vitro studies using BC cell lines (T24, 5637) and normal bladder epithelial cells (SV-HUC1).
- Quantitative assessment of ADAMTS9-AS1 and FUS expression using RT-qPCR, Western blotting, and immunohistochemistry.
- Functional assays including cell proliferation, migration, apoptosis, and cisplatin sensitivity (IC50) after transfection with ADAMTS9-AS1 and FUS overexpression plasmids.
Main Results:
- ADAMTS9-AS1 expression was significantly downregulated in BC tissues and cell lines compared to normal controls.
- FUS mRNA and protein levels were upregulated in BC.
- Overexpression of ADAMTS9-AS1 inhibited BC cell proliferation and migration, induced apoptosis, and increased cisplatin sensitivity.
- ADAMTS9-AS1 directly targets FUS, and FUS overexpression counteracted the effects of ADAMTS9-AS1.
Conclusions:
- ADAMTS9-AS1 plays a suppressive role in BC progression.
- ADAMTS9-AS1 enhances BC cell apoptosis and cisplatin sensitivity by regulating FUS.
- ADAMTS9-AS1 represents a promising therapeutic target for bladder cancer treatment.
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