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Background <p>Lung adenocarcinoma (LUAD) is the most common form of lung cancer and is often diagnosed at advanced stages. NUF2, a key component of the NDC80 kinetochore complex, is highly expressed in several malignancies, but its function and regulatory mechanism in LUAD remain unclear.</p> Methods <p>Expression profiling using TCGA, GEO datasets, and LUAD tissue microarrays revealed NUF2 dysregulation in LUAD. Functional assays (CCK-8, EdU, colony formation, Transwell, and xenograft models) were performed to assess the effects of NUF2 gain- or loss-of-function. Protein interactions were examined using immunoprecipitation and mass spectrometry. Transcriptomic sequencing and Western blotting were used to evaluate downstream signaling pathways.</p> Results <p>NUF2 expression was significantly elevated in LUAD tissues and cell lines and was positively associated with tumor stage and poor overall survival. NUF2 knockdown inhibited LUAD cell proliferation, migration, and tumor growth, whereas NUF2 overexpression enhanced malignant behaviors. Mechanistically, NUF2 interacted with and stabilized the spindle checkpoint protein BUB3 by preventing proteasomal degradation. Additionally, NUF2 activated the NF-κB signaling pathway, and BUB3 was required for this activation.</p> Conclusions <p>NUF2 promotes LUAD progression by stabilizing BUB3 and activating NF-κB signaling. Targeting the NUF2–BUB3 axis may represent a novel therapeutic strategy for LUAD.</p>

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NUF2 interacts with BUB3 and drives lung adenocarcinoma progression through activation of the NF-κB pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月6日

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  • Dingqiang Zhu,
  • Jinghui Liang,
  • Jiacheng Li,
  • Wenhao Yu,
  • Luyuan Ma,
  • Zhanpeng Tang,
  • Rongyang Li,
  • Chenghao Qu,
  • Jingyi Han,
  • Dingxin Wang,
  • Lin li,
  • Hui Tian

摘要

Background

Lung adenocarcinoma (LUAD) is the most common form of lung cancer and is often diagnosed at advanced stages. NUF2, a key component of the NDC80 kinetochore complex, is highly expressed in several malignancies, but its function and regulatory mechanism in LUAD remain unclear.

Methods

Expression profiling using TCGA, GEO datasets, and LUAD tissue microarrays revealed NUF2 dysregulation in LUAD. Functional assays (CCK-8, EdU, colony formation, Transwell, and xenograft models) were performed to assess the effects of NUF2 gain- or loss-of-function. Protein interactions were examined using immunoprecipitation and mass spectrometry. Transcriptomic sequencing and Western blotting were used to evaluate downstream signaling pathways.

Results

NUF2 expression was significantly elevated in LUAD tissues and cell lines and was positively associated with tumor stage and poor overall survival. NUF2 knockdown inhibited LUAD cell proliferation, migration, and tumor growth, whereas NUF2 overexpression enhanced malignant behaviors. Mechanistically, NUF2 interacted with and stabilized the spindle checkpoint protein BUB3 by preventing proteasomal degradation. Additionally, NUF2 activated the NF-κB signaling pathway, and BUB3 was required for this activation.

Conclusions

NUF2 promotes LUAD progression by stabilizing BUB3 and activating NF-κB signaling. Targeting the NUF2–BUB3 axis may represent a novel therapeutic strategy for LUAD.