Targeting junk DNA can help suppress cancers: Study

Targeting bits of junk DNA, known to regulate the activity of a cancer-related gene, can help suppress tumours, a new study has found.
The study led by scientists at The Scripps Research Institute (TSRI) shows how pseudogenes or junk DNA can regulate the activity of a cancer-related gene called PTEN.
Pseudogenes, which make up vast swaths of non-coding DNA, were considered part of the junk - even though they resembled genes - because they did not code for proteins.
The study shows that pseudogenes can be targeted to control PTEN's activity.
Published in the journal Nature Structural and Molecular Biology, the team's findings suggest a much larger role for pseudogenes than previously thought - a discovery that changes our understanding of the internal landscape of living cells, adding a new layer of complexity to an already crowded topography marked by multiple, overlapping, interacting gene networks.

Understanding how pseudogenes interact and control gene networks in the human body may lead to new ways of addressing diseases tied to problems that arise due to disruptions in these gene networks, said TSRI scientist Kevin Morris.

"This has improved our knowledge of how genes in cancer are regulated and how we may now be able to control them," Morris said in a statement.
The results from the new study contradict that view by showing these bits of genetic material playing a profound role in controlling the activity of human genes.
In the new work, Morris and his colleagues showed that pseudogenes can influence the activity of a human gene known as the phosphatase and tensin homolog (PTEN).

PTEN has long been implicated in cancer and is categorised as a "tumour suppressor" gene, meaning that it has the ability to arrest the growth of a tumour.
But in many forms of cancer, PTEN is shut down, allowing the tumour to grow unchecked.
Morris and his colleagues found that pseudogenes sharing sequences in common with PTEN can regulate the gene in two ways - knocking it down by suppressing the "promoter" for the PTEN gene, preventing the gene from being expressed.