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CRISPR activation screens map the genomic landscape of cancer glycome remodeling

John Daly1, Lidia Piatnitca1, Mohammed Al-Seragi1

  • 1Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, BC V6T 1Z3, Canada.

Cell Genomics
|January 29, 2026
PubMed

Insights

Cancer cells evade immune surveillance by altering cell surface sugars to engage inhibitory receptors. This study identifies key genes controlling these "cancer cloaking" glycans, revealing new immunotherapy targets.

Area of Science:

  • Immunology
  • Cancer Biology
  • Genetics

Background:

  • Cancers often increase sialic acid-containing glycans on their surface.
  • These glycans interact with inhibitory sialic acid-binding immunoglobulin-like lectin (Siglec) receptors on immune cells, enabling immune evasion.
  • The genetic basis for this cancer glycan remodeling is not well understood.

Purpose of the Study:

  • To identify genetic pathways regulating the expression of Siglec-binding glycans in cancer.
  • To understand the mechanisms of cancer immune evasion related to glycosylation.

Main Methods:

  • Utilized gain-of-function CRISPR activation (CRISPRa) screens.
  • Analyzed genetic competition between genes involved in sialylation and GlcNAcylation.
  • Investigated the role of specific genes like CD24 and GAL3ST4.

Main Results:

  • Siglec ligand expression is controlled by a genetic balance between α2-3 sialylation and GlcNAcylation pathways.
  • Overexpression of specific "professional ligands" further aids cancer cells in binding Siglecs.
  • CD24 gene expression is not essential for Siglec-10 binding.
  • Identified GAL3ST4 as a potential driver of immune evasion in glioma.

Conclusions:

  • Provides a genomic map of cancer-associated glycosylation.
  • Highlights genetic competition as a key mechanism in cancer glycan regulation.
  • Identifies novel, actionable therapeutic targets for cancer immunotherapy, including GAL3ST4 in glioma.
Keywords:
CRISPR screeningSigleccancer immune evasionglycansglycome remodelingsialic acid

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