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Ganglioside GM2 induces epithelial-mesenchymal transition (EMT) in cancer cells in a MEK/ERK/Egr1-dependent

Elora Khamrui1, Sounak Banerjee1, Subha Ray1

  • 1Department of Biological Sciences, Bose Institute, Kolkata, West Bengal, India.

The Journal of Biological Chemistry
|February 22, 2026
PubMed

Insights

Ganglioside GM2 promotes cancer cell migration and invasion by activating the MEK-ERK-Egr1 pathway. This pathway regulates epithelial-mesenchymal transition (EMT) and tumor-promoting functions, offering new therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Ganglioside GM2 is implicated in cancer progression, but its precise molecular mechanisms driving cell migration and invasion are not fully understood.
  • Understanding the signaling pathways involved in GM2-mediated tumorigenesis is crucial for developing targeted cancer therapies.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying Ganglioside GM2's role in cancer cell migration and invasion.
  • To identify the specific signaling pathways and their crosstalk involved in GM2-mediated tumorigenesis.
  • To investigate the role of the MEK-ERK-Egr1 axis in GM2-induced epithelial-mesenchymal transition (EMT) and pro-tumorigenic functions.

Main Methods:

  • Transcriptome sequencing of GM2-treated HeLa cells to identify differentially expressed genes.
  • Upregulation analysis of ERK target genes in response to exogenous GM2 in HeLa, MCF7, and SK-RC-45 cells.
  • Pharmacological inhibition of the MEK/ERK pathway using U0126 and assessment of its effects on gene expression and cell migration/invasion.
  • CRISPR-Cas9-mediated knockout of ERK1/ERK2 and Egr1 in HeLa cells to confirm pathway involvement.
  • Analysis of target gene expression (Tgfβ1, Pai-1) and mesenchymal markers following Egr1 knockout.

Main Results:

  • GM2 treatment led to differential expression of ERK target genes, with significant upregulation observed in multiple cancer cell lines.
  • Inhibition of the MEK/ERK pathway abrogated GM2-induced ERK target gene expression and reduced cancer cell migration and invasion.
  • CRISPR-Cas9-mediated knockout of ERK1/ERK2 confirmed the MEK/ERK pathway's essential role in GM2-mediated oncogenesis.
  • Knockout of Egr1 significantly reduced GM2-mediated migration/invasion and altered the expression of its targets (Tgfβ1, Pai-1) and mesenchymal markers, indicating Egr1's role in GM2-induced EMT.

Conclusions:

  • The MEK-ERK-Egr1 signaling axis is a key regulator of GM2-mediated epithelial-mesenchymal transition (EMT).
  • This pathway plays a critical role in promoting cancer cell migration, invasion, and overall tumorigenic functions.
  • Targeting the MEK-ERK-Egr1 axis presents a potential therapeutic strategy for cancers influenced by Ganglioside GM2.
Keywords:
cancerearly growth response protein 1epithelial–mesenchymal transitiongangliosidemitogen-activated protein kinase

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