ArticleCell reports2024
Functional genomics identifies N-acetyllactosamine extension of complex N-glycans as a mechanism to evade lysis by natural killer cells.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Surfaceome CRISPR activation screening uncovers ligands regulating tumor sensitivity to NK cell killing.Nature communications · 2026Article
- Inhibition of glycosphingolipid synthesis overcomes the steric hindrance of CD30 N-glycans to augment CD30-targeted immunotherapeutic efficacy.Cellular & molecular immunology · 2026Article
- From CRISPR functional genomics to synthetic interventions: engineering antiviral strategies.Journal of virology · 2026Review
- Signal peptide peptidase- and SPP-like 3-dependent shedding of α1,6-fucosyltransferase differentially affects core fucosylation.The Journal of biological chemistry · 2026Article
- The Role of Glycan Structures in Modulating GM-CSF Bioactivity: Insights from Glycoengineering.bioRxiv : the preprint server for biology · 2026Article
- Designing universal T cell therapies: strategies to evade natural killer cells.Frontiers in immunology · 2026Review
- Tumor-Expressed SPPL3 Supports Innate Antitumor Immune Responses.European journal of immunology · 2025Article
- Comprehensive self-antigen screening to assess cross-reactivity in promiscuous T-cell receptors.Frontiers in immunology · 2025Article
- GOLPH3 and GOLPH3L maintain Golgi localization of LYSET and a functional mannose 6-phosphate transport pathway.The EMBO journal · 2024Article
- Review
- The complex interplay of tumor-infiltrating cells in driving therapeutic resistance pathways.Cell communication and signaling : CCS · 2024Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Natural killer (NK) cells are primary defenders against cancer precursors, but cancer cells can persist by evading immune surveillance. To investigate the genetic mechanisms underlying this evasion, we perform a genome-wide CRISPR screen using B lymphoblastoid cells. SPPL3, a peptidase that cleaves glycosyltransferases in the Golgi, emerges as a top hit facilitating evasion from NK cytotoxicity. SPPL3-deleted cells accumulate glycosyltransferases and complex N-glycans, disrupting not only binding of ligands to NK receptors but also binding of rituximab, a CD20 antibody approved for treating B cell cancers. Notably, inhibiting N-glycan maturation restores receptor binding and sensitivity to NK cells. A secondary CRISPR screen in SPPL3-deficient cells identifies B3GNT2, a transferase-mediating poly-LacNAc extension, as crucial for resistance. Mass spectrometry confirms enrichment of N-glycans bearing poly-LacNAc upon SPPL3 loss. Collectively, our study shows the essential role of SPPL3 and poly-LacNAc in cancer immune evasion, suggesting a promising target for cancer treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.