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In this study, we performed a ChaC1-activity-directed pharmacological screening from FDA-approved drug library to identify GSH-sensitive agents, and found that ChaC1 overexpression mediated glutathione depletion largely enhanced auranofin (AUR)-induced cell death in hepatocellular carcinoma (HCC) cells
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Excessive VEGF activity promotes tumor growth, invasion, and metastasis, while insufficient signaling contributes to impaired wound healing and ischemic diseases
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Preclinical studies suggest it promotes the healing of tendons, muscle tissue, and the gastrointestinal tract
