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Breast cancer replicates brain development process

Date:
April 24, 2014
Source:
University of York
Summary:
A process that forms a key element in the development of the nervous system may also play a pivotal role in the spread of breast cancer, new research reveals. Understanding these processes is important in understanding cancer metastasis. Although the number of deaths from breast cancer is decreasing, it is still the leading cause of cancer-related death in women because of metastasis.

New research led by a scientist at the University of York reveals that a process that forms a key element in the development of the nervous system may also play a pivotal role in the spread of breast cancer.

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A research team, led by Dr Will Brackenbury, a Medical Research Council Fellow in the Department of Biology at York, has studied how voltage-gated sodium channels assist in the metastasis of cancerous tumors. These channels are found in the membranes of excitable cells, such as neurons, where they are involved in transmission of electrical impulses. However, the channels have also been found in metastatic cancer cells.

Using clinical breast cancer specimens from the Breast Cancer Campaign Tissue Bank and preclinical laboratory modelling, the researchers, including Dr Rebecca Millican-Slater, a consultant pathologist at St James University Hospital, Leeds, discovered that a sodium channel protein called Beta-one is present at high levels in breast cancer samples compared with normal tissue.

In research published in the International Journal of Cancer, they show for the first time that the increase in beta-one protein levels make tumors grow faster. They also discovered that Beta-one proteins play a significant role in enabling the cells to change shape and move, and consequently metastasise.

Understanding these processes is important in understanding cancer metastasis. Although the number of deaths from breast cancer is decreasing, it is still the leading cause of cancer-related death in women because of metastasis.

Dr Brackenbury said: "While there is no cure for metastasis, blocking the sodium channels inhibits migration and invasiveness and it may therefore be a viable therapeutic target. What is most exciting is that the mechanism by which Beta One regulates migration appears to replicate what it does in the central nervous system.

"As well as regulating electrical activity in neurons, Beta-one also regulates the migration of neurons during brain development and the breast cancer signalling mechanism seems to be the same. A process that is important in the development of the nervous system is being co-opted to play an insidious role in tumor development."

This research was funded by the Medical Research Council.

Baroness Delyth Morgan, Chief Executive at Breast Cancer Campaign, said: "The Breast Cancer Campaign Tissue Bank is vital for enabling researchers to use good quality tissue samples in their research. Dr Brackenbury's findings demonstrate how the Tissue Bank is helping drive forward research and new discoveries into what could be causing breast cancer to spread."


Story Source:

The above story is based on materials provided by University of York. Note: Materials may be edited for content and length.


Journal Reference:

  1. Michaela Nelson, Rebecca Millican-Slater, Lorna C. Forrest, William J. Brackenbury. The sodium channel β1 subunit mediates outgrowth of neurite-like processes on breast cancer cells and promotes tumour growth and metastasis. International Journal of Cancer, 2014; DOI: 10.1002/ijc.28890

Cite This Page:

University of York. "Breast cancer replicates brain development process." ScienceDaily. ScienceDaily, 24 April 2014. <www.sciencedaily.com/releases/2014/04/140424102303.htm>.
University of York. (2014, April 24). Breast cancer replicates brain development process. ScienceDaily. Retrieved November 29, 2014 from www.sciencedaily.com/releases/2014/04/140424102303.htm
University of York. "Breast cancer replicates brain development process." ScienceDaily. www.sciencedaily.com/releases/2014/04/140424102303.htm (accessed November 29, 2014).

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