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Cancer

Molecular switches in metastasis

Nature volume 406, pages 466–467 (2000)Cite this article

For patients with solid tumours, the biggest threat to survival is metastasis — the spread of tumour cells from the original growth to other sites in the body. For biologists studying cancer, a major challenge is to identify the underlying molecular changes that switch cells to a metastatic state, with the ultimate aim being to devise treatments that inhibit metastasis. Previous research has concentrated on the contribution of individual genes to metastasis. Now, gene-expression profiling, using high-density DNA microarrays, is revolutionizing our approach to studying cancer.

On page 532 of this issue, Clark et al.1 describe how they used this approach to identify several genes that are selectively upregulated in metastatic mouse and human melanoma cells compared with their non-metastatic counterparts. They find that, remarkably, overexpression of one of these genes — RhoC — can stimulate metastasis all by itself. Meanwhile, Bittner et al.2 (page 536 of this issue) have used microarrays to compare different subgroups of human melanoma, and also find a distinct pattern of gene expression in highly invasive melanoma cells.

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Figure 1: The results of Clark et al.1 and Bittner et al.2 indicate that the proteins RhoC1, fibronectin1,2 and thymosin β4 (ref. 1) are required for the metastasis, or spread, of melanoma cells.

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  1. Ludwig Institute for Cancer Research, University College London, 91 Riding House Street , London, W1W 7BS, UK

    Anne Ridley

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  1. Anne Ridley
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Correspondence to Anne Ridley.

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Ridley, A. Molecular switches in metastasis. Nature 406, 466–467 (2000). https://doi.org/10.1038/35020170

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