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<p>Long non-coding RNAs (lncRNAs) exert significant influence on the development of cancer. However, their role in colorectal cancer (CRC) is not fully clarified. The expression levels of LINC01811 in CRC samples were determined using differential expression analysis and validated by RT-qPCR assays. Transwell assays were conducted to investigate the biological function of LINC01811 in CRC. To elucidate the mechanism by which LINC01811 acts as a molecular sponge for miR-214-3p and regulates <i>YAP1</i> expression, binding site analysis, Luciferase reporter assay, RT-qPCR, and Western blotting were employed. We identified a novel oncogenic lncRNA LINC01811 in CRC tissues and cell lines. Our results showed that the suppression of LINC01811 significantly reduced CRC cell invasion and migration by regulating epithelial-mesenchymal transition-related markers, including MMP2, MMP9, vimentin, and E-cadherin in vitro. Furthermore, LINCO1811 modulated <i>YAP1</i> expression by sequestering miR-214-3p, thereby promoting CRC progression by suppressing its activity. In summary, this study identified a novel lncRNA LINC01811 involved in CRC progression through the miR-214-3p/<i>YAP1</i> axis.</p>

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Long noncoding RNA LINC01811 sponges miR-214-3p and upregulates YAP1 thereby promoting the migration and invasion of colorectal cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月10日

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  • Li Zhu,
  • Wen Shi,
  • Yiminjiang Tuoheti,
  • Guo-jie Gong,
  • Min Chen,
  • Zong-hua Liang,
  • Abuduweili Abudureheman,
  • Wei-ge Gao

摘要

Long non-coding RNAs (lncRNAs) exert significant influence on the development of cancer. However, their role in colorectal cancer (CRC) is not fully clarified. The expression levels of LINC01811 in CRC samples were determined using differential expression analysis and validated by RT-qPCR assays. Transwell assays were conducted to investigate the biological function of LINC01811 in CRC. To elucidate the mechanism by which LINC01811 acts as a molecular sponge for miR-214-3p and regulates YAP1 expression, binding site analysis, Luciferase reporter assay, RT-qPCR, and Western blotting were employed. We identified a novel oncogenic lncRNA LINC01811 in CRC tissues and cell lines. Our results showed that the suppression of LINC01811 significantly reduced CRC cell invasion and migration by regulating epithelial-mesenchymal transition-related markers, including MMP2, MMP9, vimentin, and E-cadherin in vitro. Furthermore, LINCO1811 modulated YAP1 expression by sequestering miR-214-3p, thereby promoting CRC progression by suppressing its activity. In summary, this study identified a novel lncRNA LINC01811 involved in CRC progression through the miR-214-3p/YAP1 axis.