Researchers at
Leiden University have mapped genes that cause breast cancer cells to migrate.
Aggressive tumour cells are very motile
and have dynamic 'feet' (see arrows). They can move fast. Inhibiting
the SRPK1 kinase makes the 'feet' less motile, and reduces the migration
of the tumour cells.
The Leiden toxicologists Professor Bob van de Water, Dr Wies van
Roosmalen, Dr Sylvia E. Le Dévédec and colleagues studied 1500
individual genes. They found eight, including the SRPK1 gene, that
regulate the migration of tumour cells and correlate with disease
outcome of breast cancer patients. Their findings are published in the
Journal of Clinical Investigation.
'In principle, every cell has these genes,' Van de Water
explains. ‘They always have a different degree of expression, with some
being more strongly present in tumour cells than others. We found that
in particular the presence of SRPK1 is closely linked to the potential
of breast tumour cells to migrate. This finding offers a starting point
for developing cancer medications that can prevent cells from invading
their surroundings and ultimately spreading to distant organs.'
Metastasis occurs because cancer cells go walkabout.
These eight genes were shown to control cell migration, which
is one of the causes of metastasis. Aggressive tumour cells have the
capacity to invade the tumour environment and target other parts of the
body. 'The tumour cells migrate away from the primary tumour,' Van de
Water comments. 'If the genes are expressed at a high level, the tumour
cells become more motile, which in turn increases metastasis.'
‘The genes we have identified encode for druggable molecules
known as kinases,' Van de Water explains. 'Kinases regulate the
migration of tumour cells by controlling the dynamics of what might be
called the 'feet' of the cells. These little feet allow them to be
motile and spread to other parts of the body. We are hoping to develop
new compounds that can inhibit these kinases, and reduce the chance of
metastasis. Preventing metastases and killing tumour cells at the
secondary sites is crucial for treating cancer.'