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Targeting Glycomes Sensitizes Ovarian Tumors to Immune Checkpoint Blockade II

ABSTRACT: Targeting Glycomes Sensitizes Ovarian Tumors to Immune Checkpoint Blockade II

PROVIDER: PRJNA1022481 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26226375.fastq.gz	Fastqsanger.gz
	SRR26226376.fastq.gz	Fastqsanger.gz
	SRR26226377.fastq.gz	Fastqsanger.gz
	SRR26226378.fastq.gz	Fastqsanger.gz

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Targeting Glycomes Sensitizes Ovarian Tumors to Immune Checkpoint Blockade

Project description:Targeting Glycomes Sensitizes Ovarian Tumors to Immune Checkpoint Blockade

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Targeting Glycomes Sensitizes Ovarian Tumors to Immune Checkpoint Blockade

Project description:Aberrant glycosylation is a crucial strategy employed by cancer cells to evade cellular immunity. However, homologous recombination (HR) status-dependent glycosylation has never been explored therapeutically. Here, we show that the inhibition of branched N-glycans sensitizes HR-proficient, but not HR-deficient, epithelial ovarian cancers (EOCs) to immune checkpoint blockade (ICB). In contrast to fucosylation whose inhibition sensitizes EOCs to anti-PD-L1 immunotherapy regardless of HR-status, we observe a unique enrichment of branched N-glycans on HR-proficient compared to HR-deficient EOCs. Mechanistically, BRCA1/2 transcriptionally promotes the expression of MGAT5, the enzyme responsible for catalyzing branched N-glycans. The branched N-glycans on HR-proficient tumors augment their resistance to anti-PD-L1 by enhancing its binding with PD-1 on CD8_ T cells. In orthotopic syngeneic EOC mouse models, inhibiting branched N-glycans, using 2-Deoxy-D-glucose, sensitizes HR-proficient, but not HR-deficient EOCs, to anti-PD-L1. These findings indicate branched N-glycans as promising therapeutic targets whose inhibition sensitizes HR-proficient EOCs to ICB by overcoming immune evasion

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