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Research reveals ATAD3A enhances MYC stabilization to influence glycolysis in bladder cancer, indicating new treatment options.
Our findings demonstrate that ATAD3A drives BCa progression by promoting USP10-mediated stabilization of MYC and enhancing glycolytic reprogramming. The ATAD3A-USP10-MYC axis represents a potential therapeutic target for BCa.
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Xiao et al. (2026) studied this question.
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