
This study focused on the role of oxidative stress-responsive kinase 1 (OSR1) in breast cancer metastasis and its regulatory mechanism. The researchers found that OSR1 was overexpressed in breast cancer samples and cell lines, and its high levels were associated with poor prognosis. OSR1 upregulation led to the activation of epithelial-to-mesenchymal transition (EMT), a process associated with increased metastatic capacity. Additionally, OSR1 was found to interact with and phosphorylate Smad2 and Smad3, promoting their nuclear translocation and enhancing transforming growth factor-β1 (TGF-β1) signaling, which further increased the transcription of EMT regulators. Inhibition of the OSR1-Smad2/3-TGF-β1 axis showed potential as a therapeutic strategy to counter EMT and metastasis in breast cancer.
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