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LncRNA miR143HG suppresses bladder cancer development through inactivating Wnt/β-catenin pathway by modulating
Hui Xie1, Hang Huang1, Weiping Huang1
1Department of Urology, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Abstract:
Although increasing long noncoding RNAs (lncRNAs) have been identified by high-throughput sequencing, their functions in human cancer remain largely unknown. The function of lncRNA miR143HG has not been explored before. In the present study, we found that miR143HG expression was significantly downregulated in bladder cancer tissues (BCa) compared with normal tissues. We showed that miR143HG high expression was associated with a high survival rate in BCa patients. Gain-of-function assays demonstrated that miR143HG overexpression suppressed the proliferation, arrested cell cycle progression, and attenuated migration and invasion of BCa cells in vitro. In vivo assay illustrated that ectopic expression of miR143HG inhibited BCa growth in vivo. Mechanistically, miR143HG was identified to inhibit the level of miR-1275, whereas miR-1275 directly targeted AXIN2, a negative regulator of the Wnt/β-catenin pathway. Restoration of miR-1275 or knockdown of AXIN2 significantly rescued the proliferation, migration, and invasion abilities of BCa cells. In summary, our findings demonstrated that miR143HG/miR-1275/AXIN2 axis regulates BCa development by modulating the Wnt/β-catenin pathway.
Insights
Long noncoding RNA miR143HG is downregulated in bladder cancer (BCa). Its restoration suppresses BCa cell proliferation and metastasis by inhibiting miR-1275 and the Wnt/β-catenin pathway.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long noncoding RNAs (lncRNAs) are increasingly identified, but their roles in human cancers are largely unexplored.
- The specific function of lncRNA miR143HG in bladder cancer (BCa) has not been previously investigated.
Purpose of the Study:
- To investigate the role and mechanism of lncRNA miR143HG in bladder cancer (BCa) development.
- To elucidate the regulatory pathway involving miR143HG, miR-1275, and AXIN2 in BCa.
Main Methods:
- Analysis of miR143HG expression in BCa tissues and its correlation with patient survival.
- In vitro gain-of-function assays to assess the effects of miR143HG overexpression on BCa cell proliferation, cell cycle, migration, and invasion.
- In vivo xenograft models to evaluate the impact of miR143HG on tumor growth.
- Mechanistic studies to identify the downstream targets and pathways regulated by miR143HG.
Main Results:
- miR143HG expression was significantly downregulated in BCa tissues and associated with poorer survival.
- Overexpression of miR143HG suppressed BCa cell proliferation, induced cell cycle arrest, and attenuated migration and invasion in vitro.
- Ectopic miR143HG expression inhibited BCa tumor growth in vivo.
- miR143HG inhibited miR-1275, which targets AXIN2, a negative regulator of the Wnt/β-catenin pathway. Restoration of miR-1275 or AXIN2 knockdown rescued BCa cell abilities.
Conclusions:
- The miR143HG/miR-1275/AXIN2 axis plays a critical role in regulating BCa development.
- Modulation of the Wnt/β-catenin pathway by this axis offers potential therapeutic targets for bladder cancer.
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