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C1GalT1 expression reciprocally controls tumour cell-cell and tumour-macrophage interactions mediated by galectin-3

Yangu Wan1, Kareena Adair2, Anne Herrmann3

  • 1Department of Biochemistry, Cell and Systems Biology, Institute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, UK.

Cell Death & Disease
|August 23, 2023
PubMed

Insights

Suppression of β1,3galactosyltransferase (C1GalT1) in colon cancer cells altered protein glycosylation, reducing tumor growth and cell interactions. This key enzyme impacts cancer progression and immune response.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Protein glycosylation is crucial for cell membrane proteins, yet its roles are not fully understood.
  • β1,3galactosyltransferase (C1GalT1) is vital for O-linked glycan biosynthesis and is often overexpressed in epithelial cancers.
  • C1GalT1 influences cancer cell behavior and interactions with the immune system.

Purpose of the Study:

  • To investigate the functional impact of C1GalT1 suppression on cancer cell glycosylation and its consequences.
  • To elucidate the roles of galectin-3 and MGL in C1GalT1-mediated cancer progression.
  • To assess the effect of C1GalT1 on tumor-host interactions and immune surveillance.

Main Methods:

  • Suppression of C1GalT1 expression in human colon cancer cells.
  • Analysis of protein glycosylation changes on cell membrane proteins.
  • Assessment of cancer cell proliferation, adhesion, migration, and colony formation.
  • In vivo studies using chick embryos and genetically modified mice (ME C1galt1-/-/Erb and C1galt1f/f/Erb).
  • Evaluation of galectin-3 and MGL mediated interactions and immune cell infiltration.

Main Results:

  • C1GalT1 suppression significantly altered protein glycosylation, affecting ligands for galectin-3 and MGL.
  • Reduced cancer cell proliferation, adhesion, migration, and colony formation were observed upon C1GalT1 suppression.
  • C1GalT1 suppression decreased galectin-3-mediated tumor cell interactions but enhanced MGL-mediated macrophage interactions, phagocytosis, and cytokine secretion.
  • Tumor growth was significantly reduced in C1GalT1-suppressed cells in vivo.
  • Tumor microenvironment showed increased infiltration of MGL-expressing immune cells in C1GalT1-suppressed models.

Conclusions:

  • Tumor cell C1GalT1 expression reciprocally controls tumor cell-cell and tumor-macrophage interactions via galectin-3 and MGL.
  • C1GalT1 plays a dual role in cancer development, promoting tumor growth while suppressing immune responses.
  • Overexpression of C1GalT1 in epithelial cancers is a potential mechanism for cancer promotion and immune evasion.

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