We use cookies to ensure that our site works correctly and provides you with the best experience. If you continue using our site without changing your browser settings, we'll assume that you agree to our use of cookies. Find out more about the cookies we use and how to manage them by reading our cookies policy. Hide

Mechanism that delays and repairs cancerous DNA damage discovered

microscope cancer

28 Feb 2019

Researchers at the University of Copenhagen, Denmark, have identified a mechanism that prevents natural DNA errors in our cells. These errors can lead to permanent damage to our genetic code and potentially diseases such as cancer.
Cassie Sims

Mutations occurring in human DNA can lead to fatal diseases like cancer. It is well documented that DNA-damaging processes, such as smoking tobacco or being exposed to high levels of ultraviolet (UV) light through sunburn, can lead to increased risk of developing certain forms of cancer.
Unfortunately, sometimes DNA damage can be spontaneous and occur as part of normal cellular processes such as DNA replication. Scientists have been interested in how this occurs and associated risk factors for many years.

In adult humans 250 bn cells divide and replenish each day. Damage to DNA occurs regularly during this process, but the most harmful is that which can be inherited – passed on from mother cells to newly born daughter cells. If the mother cell cannot fix the DNA it is vital that the daughter cell can, to ensure the damage isn’t passed on further.

Scientists at the University of Copenhagen have labelled a specific part of a cell that plays a vital role in DNA replication to monitor the processes occurring. This has made it possible, for the first time, to observe the fate of inherited DNA damage from mother to daughter cells. Tracking living cells under a microscope for up to days at a time is a challenging task.

The researchers found that the cell made attempts to repair the inherited damaged DNA using a ‘repair toolkit’. The key molecular part of this toolkit is an enzyme called RAD52, which now qualifies as a tumour-suppressing protein and can guard our DNA against potential cancer-causing mutations.
It is hoped that this new knowledge may help improve cancer therapy. Understanding the timing and mechanisms of DNA repair could lead to the development of new drugs and minimisation of treatment side effects.

‘Our work reveals unexpected ways in which cells deal with inherited DNA damage. With the identification of the key proteins driving this process, we have laid the foundation for investigations into potential therapeutic applications,’ says Julian Spies, postdoc at the Novo Nordisk Foundation Centre for Protein Research at the university.

DOI: 10.1038/s41556-019-0293-6 

Related Links:

Share this article