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Related Experiment Video

Updated: Apr 18, 2026

Live-3D-Cell Immunocytochemistry Assays of Pediatric Diffuse Midline Glioma

Live-3D-Cell Immunocytochemistry Assays of Pediatric Diffuse Midline Glioma

Published on: November 11, 2021

GM3 and cancer.

Sen-Itiroh Hakomori¹, Kazuko Handa

¹Division of Biomembrane Research, Pacific Northwest Research Institute, Seattle, WA, 98122, USA, hakomori@u.washington.edu.

Glycoconjugate Journal

|January 24, 2015

Summary

Reduced expression of the ganglioside GM3 is linked to cancer. Restoring GM3 synthase levels can revert cancer cells to a normal phenotype, highlighting GM3

Area of Science:

Glycobiology
Cancer Biology
Cell Signaling

Background:

Ganglioside GM3 is a key animal cell membrane component.
Malignant transformation often involves reduced GM3 expression.
GM3 influences growth factor receptor (GFR) activation.

Purpose of the Study:

To investigate the role of GM3 and GM3 synthase in cell transformation.
To explore the mechanism of GM3's effect on GFRs.
To understand GM3's function in membrane microdomains.

Main Methods:

Studied GM3 synthase mRNA levels in transformed cells.
Overexpressed GM3 synthase in transformed cells.
Utilized NEU3 sialidase to study GM3's sialosyl group role.
Analyzed GM3 complexes within glycosynaptic microdomains.

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Main Results:

GM3 synthase mRNA levels were reduced in cells transformed by v-Jun.
Overexpression of GM3 synthase reversed the transformed phenotype.
NEU3 sialidase selectively removes sialic acids from GM3.
GM3 forms complexes with signaling molecules in glycosynapses.

Conclusions:

GM3 expression is critical for maintaining normal cell phenotype.
GM3's modulation of GFRs and signaling complexes impacts cancer pathogenesis.
Targeting GM3 metabolism or function may offer therapeutic strategies.