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METASTASIS

E-selectin fills two needs for metastasis

Nature Reviews Cancer volume 19, page 301 (2019)Cite this article

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Metastasis initiation is enabled by cellular plasticity, including mesenchymal-to-epithelial transition (MET) and the gain of stem cell-like properties by cells in the metastatic organ site. However, it is unclear how these seemingly paradoxical programmes are induced. Esposito et al. showed that endothelial selectin (E-selectin) in the bone vascular niche interacts with disseminated tumour cells and controls both programmes.

Binding of E-selectin to cells is enabled by fucosyltransferases (FUT), which generate sialyl Lewis X or A (sLeX/A) tetrasaccharides on cell-surface proteins. Of the six isoforms of FUT, overexpression of FUT3, FUT5 and FUT6 significantly increased bone metastasis of bone-tropic M1a cells, a subline of SUM150 breast cancer cells — although only endogenous expression of FUT3 and FUT6 positively correlated with E-selectin binding. When M1a cells overexpressing these isoforms were subjected to a multi-organ metastasis model, FUT3 and FUT6 promoted bone metastasis, whereas primary tumour growth or lung metastasis were not affected.

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  1. Nature Reviews Cancer http://www.nature.com/nrc/

    Ulrike Harjes

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  1. Ulrike Harjes
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Correspondence to Ulrike Harjes.

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Harjes, U. E-selectin fills two needs for metastasis. Nat Rev Cancer 19, 301 (2019). https://doi.org/10.1038/s41568-019-0151-7

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