No sooner have the clocks gone forward than scientists have shed new light on the link between our biological clocks and DNA damage repair processes, essential in protecting our cells from cancer.
Studies at Cancer Research UK's London Research Institute co-funded by Breast Cancer Campaign, show that a biological clock protein called HCLK2 has an unexpected role in controlling the response of our cells to DNA damage.
Published online in Nature Cell Biology, the results build on recent studies that have demonstrated a link between DNA damage response mechanisms and proteins involved in the control of the biological clock.
Dr Simon Boulton, head of the Cancer Research UK DNA Damage Response laboratory and lead author of the research, said: "It's genuinely surprising that two seemingly unrelated processes should be so intimately linked in our cells.
"It may be that DNA repair could be scheduled by the biological clock to take place at times of reduced metabolic stress. It's a bit like road works being done overnight when there's less traffic. But such ideas are, at present, speculative and much more research needs to be carried out to understand the cross-talk between these two processes."
Our bodies have a number of ways to protect cells from damage to DNA. It's a vital task because damaged DNA can lead to genetic mutations that may contribute to the development of cancer. The "biological clock" controls the production of various proteins in the body according to the time of day.
It has been previously shown that mutations in genes vital to either the DNA damage response or the biological clock function can give rise to an increased predisposition to cancer.
The researchers discovered a link between a "clock protein" and DNA repair using the model organism, the nematode worm. Following on from this work, they demonstrated that the human version of the protein, HCLK2, directly interacts with factors that control the cellular responses to damaged DNA.
The molecular link between proteins from these two seemingly distinct processes now sheds light on why deregulation of the biological clock can lead to an increased risk of cancer.
Dr Lesley Walker, director of cancer information at Cancer Research UK, said: "It's fascinating to think that our bodies' ability to repair damaged DNA could be run by the biological clock in our brains. Proteins such as HCLK2 that are involved in our body clocks may also, therefore, have an effect on our risk of cancer and work in this area may eventually lead to improved methods of cancer treatment."
Pamela Goldberg, chief executive of Breast Cancer Campaign, said: "Breast Cancer Campaign is delighted to support Dr Boulton's ground breaking research. It's vital that we identify cancer susceptibility genes and this newly discovered candidate has the potential to be involved in a whole range of cancers. We eagerly await Dr Boulton's future studies to determine if this gene plays a role in breast cancer."