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Uncovered: How cancer-suppressing gene works

Updated on: 23 September,2015 01:28 PM IST  | 
Agencies |

Opening new opportunities for scientists to find treatments for cancer, Australian researchers have uncovered the role played by a gene which suppresses the development of cancer

Uncovered: How cancer-suppressing gene works

Cancer

Sydney: Opening new opportunities for scientists to find treatments for cancer, Australian researchers have uncovered the role played by a gene which suppresses the development of cancer.


The findings shed light on the activity of the gene WWOX.


Cancer
Representational picture


"A higher level of WWOX activity is definitely a good thing to have but, until now, the role that WWOX plays in cancer suppression has been a mystery," said Robert Richards, professor at University of Adelaide in Australia.

The researchers studied the impact of lower levels of WWOX on cells using a genetic model -- the small laboratory fly, Drosophila.

"Our research has shown that cancer cells with lower levels of WWOX had a competitive advantage over those cells with normal WWOX levels, and could outgrow them," Richards said.

"This could lead to a more aggressive cancer and worse outcomes for cancer patients -- poorer survival rates," he pointed out.

Further research showed that the WWOX gene plays a role in the altered metabolism of cancer cells which are known to use glucose differently than normal cells.

Cancer cells tend to use glucose to make more cell 'building blocks' than energy, and this is thought to help them to divide and grow.

"Low WWOX levels will allow more glucose to be used for these cancer cell 'building blocks'," Richards explained.

Researchers know that WWOX activity can be altered by targeting its enzyme activity.

"We now have a good idea of what WWOX does in cancer cells and how it acts to help suppress cancer. And we have a potential target to be able to influence that activity to change the properties of cancer cells," Richards noted.

The study was published in the journal PLOS ONE.

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