Abstract
Sphingolipids modulate the epithelial-mesenchymal transition in cancer.
Highlights
The epithelial–mesenchymal transition (EMT) allows epithelial cells to acquire biochemical and biological features of mesenchymal cells, increasing cell motility and invasiveness properties, as well as resistance to cell death
The first evidence indicating that EMT triggers SL metabolism changes was provided by Hakomori's group, showing that transforming growth factor-β (TGFβ), a well-known EMT inducer,[1] alters ganglioside metabolism in normal mouse mammary gland (NMuMG) and bladder cancer (HCV29) epithelial cell lines.[3]
TGFβinduced EMT was accompanied by a reduction of Gg4 and GM2, which belong to the 0- and a-series gangliosides, respectively.[3]
Summary
The epithelial–mesenchymal transition (EMT) allows epithelial cells to acquire biochemical and biological features of mesenchymal cells, increasing cell motility and invasiveness properties, as well as resistance to cell death.
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