IndraLab

Statements


USP13 activates METTL3. 6 / 6
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"Collectively, our study results indicate that USP13 promotes glycolysis and tumor progression in OS by stabilizing METTL3, thereby stabilizing ATG5 mRNA and facilitating autophagy in OS."

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"Silencing of USP13 significantly accelerated METTL3 degradation while upregulation of USP13 obviously inhibited METTL3 degradation (Fig. 3h, i)."

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"Wang et al. reveal that injecting Spautin-1 into mice bearing xenografts effectively inhibits the USP13-enhanced stabilization of METTL3, subsequently reducing the stability of ATG5 mRNA and thereby curbing tumor proliferation and metastasis 130."

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"Ectopically expressed K488R of METTL3 significantly promoted cell proliferation and glycolysis, while USP13 knockdown decreased cell proliferation and glycolysis with WT METTL3 rather than K488R METTL3, which indicated that mutation of K488 of METTL3 promoted cell proliferation and glycolysis and abolished USP13 depletion-induced proliferation and glycolysis suppression (Fig. 4i-n)."

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"Collectively, our results demonstrated that pharmacological inhibition of USP13 effectively inhibit the malignancy of OS by promoting METTL3 destabilization."

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"USP13 promotes glycolysis and progression in OS by binding to and stabilizing METTL3."