Related Experiment Video

Updated: Apr 3, 2026

Glycan Node Analysis: A Bottom-up Approach to Glycomics
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Glycan Node Analysis: A Bottom-up Approach to Glycomics

Published on: May 22, 2016

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Mining cancer genomes for copy number alterations identifies glycosylation enzymes as oncogenic drivers

Pranoy Sahu1, Francesco Russo1, Domenico Russo1

  • 1Institute of Endotypes in Oncology, Metabolism and Immunology "G. Salvatore," National Research Council of Italy, Naples 80131, Italy.

Proceedings of the National Academy of Sciences of the United States of America
|April 1, 2026
PubMed

Insights

Researchers identified novel cancer-driving genes in glycan biosynthesis. They found that B4GALT5 acts as a glyco-oncogene, promoting cancer growth and survival, offering new therapeutic targets.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Altered cell-surface glycans are recognized cancer biomarkers.
  • No genes within glycan biosynthesis machinery have been definitively classified as oncogenes.
  • Identifying oncogenes within this pathway is crucial for understanding cancer dependencies and improving clinical decisions.

Purpose of the Study:

  • To develop a pipeline for identifying copy number alteration (CNA)-based driver genes in glycan biosynthesis.
  • To discover novel glyco-oncogenes and validate their role in cancer.
  • To investigate the functional role of B4GALT5 in cancer progression and survival.

Main Methods:

  • Developed a bioinformatic-experimental pipeline to identify CNA-driven genes, distinguishing drivers from passengers.
  • Focused on the glycosphingolipid (GSL) biosynthetic pathway.
  • Validated B4GALT5 as a glyco-oncogene through functional and mechanistic studies, including pathway inhibition and signaling analysis.

Main Results:

  • The pipeline successfully identified known oncogenes and tumor suppressors, alongside novel candidates including glyco-oncogenes.
  • Genomic amplification of B4GALT5 was confirmed as a driver of cancer proliferation, oncogene addiction, and poor prognosis.
  • B4GALT5 was shown to enhance cancer cell survival under anchorage-independent conditions by promoting integrin-Src signaling.

Conclusions:

  • Glycosylation enzymes represent a druggable class of oncogenes.
  • B4GALT5 is a validated glyco-oncogene whose amplification drives cancer progression.
  • Targeted inhibition of the B4GALT5 pathway can reverse oncogenic effects, offering potential therapeutic strategies.
Keywords:
copy-number alterationsglycosphingolipidsgolgioncogenes

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