IndraLab

Statements

USP13 activates glycolytic process. 8 / 8
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"USP13 promotes glycolysis and progression in OS by binding to and stabilizing METTL3."
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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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"Next, we investigated the role of METTL3 in the mechanism by which USP13 promotes glycolysis and progression of OS cells via lentiviral-mediated METTL3 overexpression in USP13-silenced 143B cells and METTL3 silencing in USP13-upregulated HOS cells."
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"Using various in vitro and in vivo functional experiments, USP13 was demonstrated to promote glycolysis and tumor progression in OS."
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"Despite this, the diverse roles of autophagy in tumor biology should be explored more comprehensively.Collectively, our findings in the present study showed that USP13 promotes aerobic glycolysis and OS development by binding to, stabilizing and reducing ubiquitination and degradation of the m A writer METTL3 at K488 by removing K48-linked ubiquitin chains., which subsequently increases the m A modification of ATG5 mRNA and stabilizes it, thus promoting oncogenic autophagy."
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"USP13 was found to upregulate in osteosarcoma (OS) specimens and promote OS progression through regulating aerobic glycolysis."
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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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"USP13 promotes glycolysis and cell proliferation in OS."
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