ArticleThe Journal of biological chemistry2026
Ganglioside GM2 induces epithelial-mesenchymal transition (EMT) in cancer cells in a MEK/ERK/Egr1-dependent transcriptional program.
Article in The Journal of biological chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Ganglioside GM2 plays a critical role in cancer cell migration and invasion, although the intricate molecular mechanism remains elusive. This study provides a novel insight on the underlying signaling pathways and their cross talk involved in GM2-mediated tumorigenesis. Transcriptome sequencing displayed differential expression of ERK (extracellular signal-regulated kinase) target genes in GM2-treated HeLa cells. Results further showed significant upregulation of the ERK target gene expression in HeLa, MCF7 and SK-RC-45 cells in the presence of exogenous GM2. Inhibition of the MAPKK (mitogen-activated protein kinase kinase), MEK pathway with small molecule inhibitor U0126 abrogated target gene expression through the reduction in the phosphorylation level of ERK1/2 and caused functional reduction of GM2-induced migration and invasion of HeLa cells. CRISPR-Cas9-mediated knockout of ERK1 and ERK2 in HeLa cells rendered the downregulation of ERK-target gene expression in response to exogenous GM2, confirming the involvement of MEK/ERK pathway in the regulation of GM2-mediated oncogenesis. Moreover, functional knockout of Egr1 (early growth response protein 1, an ERK-target) caused significant reduction in the GM2-mediated migration/invasion of HeLa cells and induction in expression of its targets, Tgfβ1 (transforming growth factor beta 1) and Pai-1 (plasminogen activator 1). Finally, Egr1 KO in HeLa cells further reduced the induction of mesenchymal marker expression in the presence of GM2, thereby confirming the role of Egr1 in GM2-induced epithelial-mesenchymal transition (EMT) process. Taken together, this study identified MEK-ERK-Egr1 axis as an important regulatory signaling in GM2-mediated EMT and pro-tumorigenic functions.
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