Metabolically encoded cell-surface glycoRNA remodeling enhances antitumor immunity
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Glycolysis in breast cancer cells drives c-Myc-dependent repression of DTWD2, reducing acp3U attachment sites needed for RNA glycosylation and remodeling cell-surface glycoRNA. Loss of DTWD2-impaired glycoRNA weakens Toll-like receptor signaling activation, dendritic cell maturation and CD8+ T cell responses, while reversing aerobic glycolysis to restore glycoRNA improves the antitumor efficacy of PD-1 blockade. Lower glycoRNA abundance tracks with tumor stage and unfavorable prognosis, positioning glycoRNA as a regulator of antitumor immunity and a progression biomarker.
Excerpted from biorxiv.org
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- biorxiv.orgPickMetabolically encoded cell-surface glycoRNA remodeling enhances antitumor immunity
Glycolysis in breast cancer cells drives c-Myc-dependent repression of DTWD2, reducing acp3U attachment sites needed for RNA glycosylation and remodeling cell-surface glycoRNA. Loss of DTWD2-impaired glycoRNA weakens Toll-like receptor signaling activation, dendritic cell maturation and CD8+ T cell responses, while reversing aerobic glycolysis to restore glycoRNA improves the antitumor efficacy of PD-1 blockade. Lower glycoRNA abundance tracks with tumor stage and unfavorable prognosis, positioning glycoRNA as a regulator of antitumor immunity and a progression biomarker.
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