The lncRNA ELF3-AS1 promotes bladder cancer progression by interaction with Krüppel-like factor 8.
[No authors listed]
摘要
Accumulating evidence has shown the critical role of long non-coding RNAs (lncRNAs) during cancer progression. However, the involvement of ELF3-AS1 in bladder cancer (BC) remains largely unclear. By lncRNA profiling, we identified ELF3-AS1 as a novel oncogenic lncRNA during bladder cancer development. ELF3-AS1 was highly expressed in bladder cancer and correlated with poor prognosis. ELF3-AS1 could increase viability and migration of bladder cancer cells in vitro and promoted xenograft tumor growth in vivo. Furthermore, ELF3-AS1 could interact with KLF8 to stabilize KLF8 by protecting it from proteasome-mediated degradation. KLF8 in turn could bind ELF3-AS1 promoter and transactivate ELF3-AS1 expression. The positive feedback loop between ELF3-AS1 and KLF8 enhanced KLF8 signaling by increasing MMP9 expression. Collectively, our study has unraveled a novel mechanism of ELF3-AS1-mediated oncogenesis in bladder cancer by reinforcement of ELF3-AS1/KLF8 signaling with potential implications for therapeutic intervention.
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基因功能
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原始数据
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文献解读
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