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<p>Aberrant overexpression of AURKA (aurora kinase A) is strongly associated with various malignancies. However, limited research exists regarding its clinical significance and pathogenic mechanisms in lung adenocarcinoma. This study elucidates clinical correlations and provides experimental evidence supporting AURKA’s potential as a therapeutic target for lung adenocarcinoma (LUAD). We analyzed AURKA expression levels and prognostic value using data from TCGA and GEO databases. qRT-PCR compared AURKA expression in LUAD tissues and adjacent normal specimens. siRNA-mediated knockdown efficiency was verified through western blotting and qRT-PCR. Cellular proliferation was assessed via CCK-8 assays and tumor ball assay, while migration capacity was evaluated using transwell chambers. Flow cytometry analyzed cell cycle progression and apoptosis. Phosphoproteomic sequencing identified downstream pathways, with western blot validation of key targets. The changes of tight junctions were observed by transmission electron microscopy, fluorescein isothiocyanate dextran 4&#xa0;kDa (FD4) permeation experiment and immunofluorescence. A subcutaneous xenograft model in nude mice evaluated AURKA’s in vivo tumorigenic effects. Our work illustrated that Elevated AURKA expression correlated significantly with poor LUAD prognosis. AURKA silencing markedly suppressed A549 cell proliferation and migration capacity while inducing G2/M phase arrest and apoptosis. Phosphorylated protein sequencing shows that AURKA knockdown is closely related to Cortactin (CTTN) mediated tight junction. Meanwhile, Xenograft models demonstrated that AURKA knockdown substantially inhibited tumor growth and metastatic progression. It was concluded that AURKA serves as a prognostic biomarker in LUAD. Mechanistically, AURKA promotes tumor progression through Cortactin phosphorylation-mediated tight junction disruption. Our findings establish AURKA inhibition as a promising therapeutic strategy for LUAD management.</p>

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AURKA modulates tight junction functionality to influence the proliferation and metastasis of lung adenocarcinoma

  • 期刊论文

  • 发表日期：

    2025年11月7日

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  • Yuan Mi,
  • Junjie Mao,
  • Xuzhe Li,
  • Zilin Wang,
  • Xin Zuo,
  • Zihan Chang,
  • Ruibo Wang,
  • Lantao Wang,
  • Lei Wang

摘要

Aberrant overexpression of AURKA (aurora kinase A) is strongly associated with various malignancies. However, limited research exists regarding its clinical significance and pathogenic mechanisms in lung adenocarcinoma. This study elucidates clinical correlations and provides experimental evidence supporting AURKA’s potential as a therapeutic target for lung adenocarcinoma (LUAD). We analyzed AURKA expression levels and prognostic value using data from TCGA and GEO databases. qRT-PCR compared AURKA expression in LUAD tissues and adjacent normal specimens. siRNA-mediated knockdown efficiency was verified through western blotting and qRT-PCR. Cellular proliferation was assessed via CCK-8 assays and tumor ball assay, while migration capacity was evaluated using transwell chambers. Flow cytometry analyzed cell cycle progression and apoptosis. Phosphoproteomic sequencing identified downstream pathways, with western blot validation of key targets. The changes of tight junctions were observed by transmission electron microscopy, fluorescein isothiocyanate dextran 4 kDa (FD4) permeation experiment and immunofluorescence. A subcutaneous xenograft model in nude mice evaluated AURKA’s in vivo tumorigenic effects. Our work illustrated that Elevated AURKA expression correlated significantly with poor LUAD prognosis. AURKA silencing markedly suppressed A549 cell proliferation and migration capacity while inducing G2/M phase arrest and apoptosis. Phosphorylated protein sequencing shows that AURKA knockdown is closely related to Cortactin (CTTN) mediated tight junction. Meanwhile, Xenograft models demonstrated that AURKA knockdown substantially inhibited tumor growth and metastatic progression. It was concluded that AURKA serves as a prognostic biomarker in LUAD. Mechanistically, AURKA promotes tumor progression through Cortactin phosphorylation-mediated tight junction disruption. Our findings establish AURKA inhibition as a promising therapeutic strategy for LUAD management.