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Background <p>Accumulating evidence indicates that long non-coding RNA (lncRNA) miR17HG plays important roles in tumorigenesis in various cancers. However, its underlying effect on bladder cancer (BC) remains to be explored.</p> Objective <p>This study aims to elucidate the function and molecular mechanisms of lncRNA miR17HG in the proliferation and metastasis of BC.</p> Methods <p>BC tissues and matched para-cancerous tissues were collected from our hospital. Oncology functional assays, quantitative reverse-transcription polymerase chain reaction, and western blotting were conducted to confirm the role of lncRNA miR17HG in BC development. The interations among lncRNA miR17HG, miR-144-3p and AXIN2 were verified via luciferase reporter assay. Nude mouse subcutaneous tumor models were established to investigate the effect of lncRNA miR17HG on BC tumor growth.</p> Results <p>LncRNA miR17HG and miR-144-3p were significantly upregulated, while AXIN2 was downregulated in BC tissues. Knockdown of lncRNA miR17HG or inhibition of miR-144-3p suppressed cell proliferation, migration and invasion, whereas miR-144-3p mimic exerted the opposite effects. Mechanistically, lncRNA miR17HG sponged miR-144-3p to regulate the expression of AXIN2. Furthermore, lncRNA miR17HG knockdown effectively suppressed tumor xenograft growth in mice.</p> Conclusion <p>In summary, this study identifies a novel lncRNA miR17HG/miR-144-3p/AXIN2 pathway in BC and demonstrate that this regulatory axis may serve as a promising therapeutic target for BC.</p>

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LncRNA miR17HG promotes tumor progression through AXIN2 by sponging miR-144-3p in bladder cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月21日

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  • Qiong Chen,
  • Keming Wu,
  • Bing Cai,
  • Xiuxiu Yu,
  • Xiaoyan Zhang,
  • Yu Yang

摘要

Background

Accumulating evidence indicates that long non-coding RNA (lncRNA) miR17HG plays important roles in tumorigenesis in various cancers. However, its underlying effect on bladder cancer (BC) remains to be explored.

Objective

This study aims to elucidate the function and molecular mechanisms of lncRNA miR17HG in the proliferation and metastasis of BC.

Methods

BC tissues and matched para-cancerous tissues were collected from our hospital. Oncology functional assays, quantitative reverse-transcription polymerase chain reaction, and western blotting were conducted to confirm the role of lncRNA miR17HG in BC development. The interations among lncRNA miR17HG, miR-144-3p and AXIN2 were verified via luciferase reporter assay. Nude mouse subcutaneous tumor models were established to investigate the effect of lncRNA miR17HG on BC tumor growth.

Results

LncRNA miR17HG and miR-144-3p were significantly upregulated, while AXIN2 was downregulated in BC tissues. Knockdown of lncRNA miR17HG or inhibition of miR-144-3p suppressed cell proliferation, migration and invasion, whereas miR-144-3p mimic exerted the opposite effects. Mechanistically, lncRNA miR17HG sponged miR-144-3p to regulate the expression of AXIN2. Furthermore, lncRNA miR17HG knockdown effectively suppressed tumor xenograft growth in mice.

Conclusion

In summary, this study identifies a novel lncRNA miR17HG/miR-144-3p/AXIN2 pathway in BC and demonstrate that this regulatory axis may serve as a promising therapeutic target for BC.