Taking Control of Gene Regulators to Stop Breast Cancer’s Spread

Once breast cancer spreads, or metastasizes, to other parts of the body, it becomes much more difficult to treat. To improve options for women with metastatic breast cancer, scientists are trying to figure out how and why breast cancer spreads. 

Early-stage research suggests that it may be possible to stop the spread of breast cancer by changing the activity of molecules that are helping control whether certain genes get turned on or turned off. If the wrong combination of genes gets turned on – or off – cancer can spread.

Some of the molecules that play a role in turning genes on and off are called chromatin remodeling complexes. These complexes consist of scaffolds that recruit other proteins to do the work of turning genes on and off. The scaffolds can be compared to a corporate recruiter, whose responsibility is to hire the right people to fill specific jobs. If the recruiter doesn’t fill the jobs, the company can’t grow and expand. Similarly, if the scaffolds can’t recruit proteins to do the job of turning genes on and off, then the tumor cells can’t grow and spread.

In breast cancer, one specific type of complex may be the key to stopping metastasis – it is called SIN3. “The SIN3 complex plays a role in regulating breast cancer metastasis,” says Douglas Hurst, Ph.D., a researcher who is studying SIN3 at the University of Alabama at Birmingham. Hurst is investigating SIN3 with the help of funding from the American Cancer Society and the HOPE (Health Opportunity through Partnership in Education) Foundation, a non-profit organization, associated with Washington National Insurance Company of Carmel, Indiana.

“There is a group of researchers at Mount Sinai Hospital that have developed an inhibitor of the SIN3 complex and showed that with it you can stop breast cancer progression and invasion,” says Hurst. But Hurst says the science of SIN3 has recently become much more interesting and complex. “It turns out there is a SIN3A and a SIN3B that have completely different functions.”

“Our recent studies have shown that one looks like it promotes breast cancer metastasis and the other one inhibits breast cancer metastasis,” says Hurst. “What we are trying to do now is figure out what is different about the proteins that SIN3A and SIN3B are recruiting; this information will help us understand why one complex is more likely to promote the spread of breast cancer and the other is more likely to inhibit its spread.”

Since the SIN3 complexes recruit all different kinds of proteins, Hurst wants to figure out exactly which of these proteins are leading to breast cancer metastasis so a drug could be created to target just those offending proteins. His hope is that a more specific drug will be more effective.

“We have analyzed the targets (or genes that are turned on and off) of the SIN3A and SIN3B complexes and have found quite a few differences – the next step is to answer the question of what proteins in the SIN3A and SIN3B complexes are different to help us understand potential targets,” says Hurst.

Hurst hopes that his research will “pave the way for future projects specifically targeting the activity of these complexes for anti-metastatic treatment.”

VIDEO: Go Inside Dr. Hurst's Lab

Stopping Breast Cancer’s Spread Through Gene Regulators

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