Scholarlink

<p>Karyopherin subunit alpha 2 (<i>KPNA2</i>) has been implicated in a variety of human diseases, particularly cancer. This study aimed to elucidate the role of <i>KPNA2</i> in the development and progression of gastric cancer (GC). Bioinformatics analyses revealed that <i>KPNA2</i> expression was significantly higher in GC tissues, and qRT-PCR, western blotting, and immunohistochemistry subsequently validated these findings. To establish a clearer connection between bioinformatics findings and functional validation, in vitro experiments were performed in GC cell lines, in which silencing of <i>KPNA2</i> significantly inhibited cell proliferation, migration, and invasion. These inhibitory effects were further confirmed in mouse xenograft models. <i>KPNA2</i> depletion impaired DNA replication, induced S-phase cell cycle arrest, and significantly enhanced apoptosis in GC cells. Molecular analyses further demonstrated that <i>KPNA2</i> downregulation suppressed β-catenin signaling pathway activation and inhibited epithelial-mesenchymal transition. These results suggest that <i>KPNA2</i> facilitates GC cell proliferation, cell cycle progression, resistance to apoptosis, and metastatic behavior by activating the β-catenin/EMT axis. Therefore, <i>KPNA2</i> may serve as a potential therapeutic target for gastric cancer.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

KPNA2 knockdown suppresses gastric cancer progression through modulation of the β-catenin/EMT signaling axis, inducing cell cycle arrest, apoptosis, and reduced metastatic capacity

  • 期刊论文

  • 发表日期：

    2026年7月6日

查看全文
  • Haoyu Zhu,
  • Tianli Niu,
  • Shichun Feng,
  • Chao Shi,
  • Chong Tang,
  • Fei Wang

摘要

Karyopherin subunit alpha 2 (KPNA2) has been implicated in a variety of human diseases, particularly cancer. This study aimed to elucidate the role of KPNA2 in the development and progression of gastric cancer (GC). Bioinformatics analyses revealed that KPNA2 expression was significantly higher in GC tissues, and qRT-PCR, western blotting, and immunohistochemistry subsequently validated these findings. To establish a clearer connection between bioinformatics findings and functional validation, in vitro experiments were performed in GC cell lines, in which silencing of KPNA2 significantly inhibited cell proliferation, migration, and invasion. These inhibitory effects were further confirmed in mouse xenograft models. KPNA2 depletion impaired DNA replication, induced S-phase cell cycle arrest, and significantly enhanced apoptosis in GC cells. Molecular analyses further demonstrated that KPNA2 downregulation suppressed β-catenin signaling pathway activation and inhibited epithelial-mesenchymal transition. These results suggest that KPNA2 facilitates GC cell proliferation, cell cycle progression, resistance to apoptosis, and metastatic behavior by activating the β-catenin/EMT axis. Therefore, KPNA2 may serve as a potential therapeutic target for gastric cancer.