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Long non-coding RNA NEAT1 promotes bladder progression through regulating miR-410 mediated HMGB1
Guang Shan1, Tian Tang2, Yue Xia1
1Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|November 18, 2019
Summary
Long noncoding RNA NEAT1 promotes bladder cancer by regulating the miR-410/HMGB1 axis. NEAT1 knockdown inhibits tumor growth and proliferation, while its overexpression accelerates bladder cancer development.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long noncoding RNA NEAT1 is implicated as an oncogene in various cancers.
- The specific role of NEAT1 in bladder cancer pathogenesis remains largely unexplored.
Purpose of the Study:
- To investigate the function and biological role of NEAT1 in bladder cancer.
- To elucidate the molecular mechanisms underlying NEAT1's involvement in bladder cancer progression.
Main Methods:
- Assessed NEAT1 expression levels in bladder cancer cell lines.
- Performed in vitro knockdown and overexpression studies of NEAT1.
- Conducted in vivo experiments using nude mouse models.
- Utilized bioinformatics analysis to predict and validate downstream targets (miR-410, HMGB1).
- Employed dual-luciferase reporter assays to confirm regulatory interactions.
Main Results:
- NEAT1 expression was significantly elevated in bladder cancer cells.
- NEAT1 knockdown suppressed cell proliferation, induced apoptosis, and caused cell cycle arrest.
- NEAT1 overexpression reversed these effects.
- In vivo studies demonstrated NEAT1 knockdown inhibited tumor growth, while overexpression promoted it.
- NEAT1 was found to target miR-410, which in turn targets HMGB1, establishing the NEAT1/miR-410/HMGB1 axis.
Conclusions:
- The NEAT1/miR-410/HMGB1 axis plays a critical role in bladder cancer development and progression.
- NEAT1 acts as an oncogene in bladder cancer, potentially through the regulation of miR-410 and HMGB1.
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