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

Authors

Haoyu Zhu, Tianli Niu, Shichun Feng, Chao Shi, Chong Tang, Fei Wang

Published in

Journal of molecular histology. Volume 57. Issue 4. Jul 06, 2026. Epub Jul 06, 2026.

Abstract

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.

PMID:
42406150
Bibliographic data and abstract were imported from PubMed on 06 Jul 2026.

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