ArticleThe Kaohsiung journal of medical sciences2026
DARS2 Promotes Tumorigenesis and Metastasis by Activating PI3K/Akt/GSK-3β/β-Catenin Signaling Pathway in Breast Cancer.
Article in The Kaohsiung journal of medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Aspartyl-tRNA synthetase 2 (DARS2), the mitochondrial enzyme responsible for aminoacylation of aspartyl-tRNA, is traditionally known for its effect on protein synthesis. Recently, DARS2 is reported to be implicated in tumorigenesis. However, its specific effect on breast cancer (BC) is poorly understood. The present work employed bioinformatics tools for analyzing DARS2 expression among BC patients and its association with clinicopathological characteristics and patient prognosis. We evaluated DARS2 expression within BC cells and tissues and assessed how DARS2 knockdown or PI3K pathway activation affected cell growth, migration, invasion, apoptosis, as well as cell cycle progression. Mechanistically, we analyzed how DARS2 regulated the PI3K/Akt/GSK-3β/β-catenin pathway. Additionally, a xenograft tumor model was constructed to validate our in vitro findings. According to our observations, DARS2 expression significantly increased in BC cells and tissues. Knockdown of DARS2 markedly suppressed cell growth, invasion, migration, and epithelial-mesenchymal transition (EMT), but enhanced their apoptosis. Mechanistic studies revealed that DARS2 knockdown suppressed the PI3K/Akt/GSK-3β/β-catenin pathway, whereas PI3K pathway activation with 740Y-P reversed the impacts of DARS2 knockdown. In vivo experimental results further verified that DARS2 suppression significantly suppressed tumor growth and metastasis through downregulating the PI3K/Akt/GSK-3β/β-catenin pathway. Collectively, these results indicate that DARS2 promotes the growth, migration, invasion, and EMT of BC cells by regulating the PI3K/Akt/GSK-3β/β-catenin signaling pathway.
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