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DARS2 Promotes Tumorigenesis and Metastasis by Activating PI3K/Akt/GSK-3β/β-Catenin Signaling Pathway in Breast
1School of Stomatology and Ophthalmology, Xianning Medical College, Hubei University of Science and Technology, Xianning, Hubei, China.
Aspartyl-tRNA synthetase 2 (DARS2) promotes breast cancer growth and metastasis by activating the PI3K/Akt/GSK-3β/β-catenin pathway. Suppressing DARS2 inhibits tumor progression and epithelial-mesenchymal transition (EMT).
Area of Science:
- Molecular Biology
- Biochemistry
- Oncology
Background:
- Aspartyl-tRNA synthetase 2 (DARS2) is a mitochondrial enzyme essential for protein synthesis.
- Emerging evidence suggests DARS2 involvement in tumorigenesis, but its role in breast cancer (BC) remains unclear.
Purpose of the Study:
- To investigate the role of DARS2 in breast cancer progression.
- To elucidate the molecular mechanisms by which DARS2 influences BC cell behavior and patient prognosis.
Main Methods:
- Bioinformatic analysis of DARS2 expression in BC patients.
- In vitro studies involving DARS2 knockdown and PI3K pathway activation in BC cells.
- Assessment of cell growth, migration, invasion, apoptosis, and cell cycle.
- Mechanistic analysis of the PI3K/Akt/GSK-3β/β-catenin pathway.
- In vivo xenograft tumor model validation.
Main Results:
- DARS2 expression is significantly upregulated in BC cells and tissues.
- DARS2 knockdown suppressed BC cell growth, migration, invasion, and epithelial-mesenchymal transition (EMT), while promoting apoptosis.
- DARS2 regulates the PI3K/Akt/GSK-3β/β-catenin pathway; PI3K activation reversed DARS2 knockdown effects.
- In vivo studies confirmed that DARS2 suppression inhibits tumor growth and metastasis.
Conclusions:
- DARS2 promotes breast cancer progression, including growth, migration, invasion, and EMT.
- DARS2 exerts its oncogenic effects by regulating the PI3K/Akt/GSK-3β/β-catenin signaling pathway.
- DARS2 represents a potential therapeutic target for breast cancer treatment.
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