MicroRNA causes "double whammy" of metastasis and angiogenesis in breast cancer

Primary tumours are not the big killers, it's the secondary tumours that account for 90 per cent of the mortality of cancer.

Now a new study out of the U.S. has shown that the microRNA, miR-9, plays a significant role in metastasis, both enabling cells to spread to other parts of the body as well as encouraging tumour angiogenesis.

The researchers found that miR-9 is upregulated in breast cancer cells and this microRNA then downregulates a protein, E-cadherin. This protein normally acts as a kind of 'glue' for keeping epithelial cells together which prevents the spread of cancerous cells.

Thus, when miR-9 is upregulated, and E-cadherin downregulated, the tumour cells are able to spread to other parts of the body.

Furthermore, miR-9 also plays a role in increasing angiogenesis, or blood vessel growth, which increases blood supply in the tumour, aiding its continued growth.

The study looked at mice and found that miR-9 overexpression in non-metastatic breast cancer cells enabled these cells to become metastatic.

Conversely, inhibiting miR-9 through the use of a 'miRNA sponge' in highly malignant cells served to inhibit metastasis.

It's known that miR-9 expression is controlled by the oncogene, Myc, and this occurs not only in mouse cancers but human breast cancer as well.

The research is paralleled by studies conducted by Greg Goodall and Yeesim Khew-Goodall at the Centre for Cancer Biology in Adelaide, who has been investigating the role of another family of microRNAs, miR-200, on metastasis.

Writing in Nature Cell Biology, Goodall calls the action of miR-9 a "double whammy, not only priming cancer cells for EMT and invasion, but also promoting angiogenesis, thus helping the tumour to grow, and providing a nearby escape route for migrating cancer cells."

A deeper understanding of the roles played by Myc and microRNAs could lead to new treatments to prevent metastasis, and thus the deaths caused by secondary tumours.

The research was published in Nature Cell Biology and was led by Robert A. Weinberg from the Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, U.S..