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<p>Aspartate/asparagine-β-hydroxylase (ASPH), a type II transmembrane α-ketoglutarate-dependent hydroxylase, is frequently overexpressed in various cancers. However, its role in lung adenocarcinoma (LUAD) remains unclear. Here, we analyzed ASPH expression in LUAD and normal lung tissues using bioinformatic tools, and evaluated its association with clinicopathological characteristics and patient prognosis. High ASPH expression correlated with advanced disease and poor survival, and served as an independent prognostic factor. Functional assays, including Transwell, scratch healing, and murine lung metastasis models, demonstrated that ASPH promotes LUAD cell migration and metastasis. The potential molecular mechanisms by which ASPH exerts its function in LUAD were explored by transcriptome sequencing analysis and immunoprecipitation combined with mass spectrometry (IP-MS). Further analysis showed that ASPH enhances activation of the MAPK and Notch signaling pathways through RUVBL2 interaction. Collectively, our findings suggest that ASPH contributes to LUAD progression by engaging RUVBL2 and activating key oncogenic signaling cascades, highlighting its potential as a prognostic biomarker and therapeutic target.</p>

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ASPH interacts with RUVBL2 to promote tumor metastasis in lung adenocarcinoma via MAPK and Notch signaling pathways

  • 期刊论文

  • 发表日期：

    2025年12月27日

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  • Chuhong Huang,
  • Huihao Lu,
  • Jiali Dong,
  • Yanming Lin,
  • Yuting Chen,
  • Zhixiong Yang,
  • Wenmei Su,
  • Zhen Cheng

摘要

Aspartate/asparagine-β-hydroxylase (ASPH), a type II transmembrane α-ketoglutarate-dependent hydroxylase, is frequently overexpressed in various cancers. However, its role in lung adenocarcinoma (LUAD) remains unclear. Here, we analyzed ASPH expression in LUAD and normal lung tissues using bioinformatic tools, and evaluated its association with clinicopathological characteristics and patient prognosis. High ASPH expression correlated with advanced disease and poor survival, and served as an independent prognostic factor. Functional assays, including Transwell, scratch healing, and murine lung metastasis models, demonstrated that ASPH promotes LUAD cell migration and metastasis. The potential molecular mechanisms by which ASPH exerts its function in LUAD were explored by transcriptome sequencing analysis and immunoprecipitation combined with mass spectrometry (IP-MS). Further analysis showed that ASPH enhances activation of the MAPK and Notch signaling pathways through RUVBL2 interaction. Collectively, our findings suggest that ASPH contributes to LUAD progression by engaging RUVBL2 and activating key oncogenic signaling cascades, highlighting its potential as a prognostic biomarker and therapeutic target.