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Disruption of Sleep Cycle Linked To Cancer Development

The disruption of the sleep cycle might lead to the development of cancer. It was shown by researchers of a new study that a molecule involved in regulating the circadian clock is modified in function when the sleep cycle is disrupted. As a result, another protein which is a tumour suppressor is affected by the change and uncontrolled cell division thus occurs.

Humans are programmed to find rest during sleep. Though we remain seemingly inactive when we fly off to dream-world, it is indeed a process that is crucial to our very existence. We, creatures, slumber and sleep – it is beyond us. If this critically important stage of our daily routines is disrupted, bitter consequences are likely to follow. Scientists have suggested that disturbed sleep cycles might impact negatively on cancer development. A new study has recently brought more insight into the matter.

Sleep linked with cancer development?

The researchers of the new study might have worked out the mechanism linking sleep patterns and cancer progression. It was found that a protein regulating the sleep cycle (circadian rhythm), known as hPer2, is also associated with protection against cancer. When our sleep cycle is modified, the regulating proteing hPer2 changes in function, and this might lead to cancer.

Mechanism linking hPer2 with cancer?

hPer2 interacts with another protein which is a tumour suppressor, the protein human p53 (hp53). The two proteins engage in interactions to regulate cell division.

As a consequence, when the gene for hPer2 was suppressed in the study experiments, the sleep cycle grew abnormal, and, at the same time, uncontrolled cell division occured.

The authors explained that:

When hPer2 is non-functional because it is either mutated or somehow modified, then it is unable to do its job and prevent the cells from dividing at certain times of the day. This is particularly a problem in cases where tumor suppressor genes are mutated, as it happens in more than 80% of all cancer cases.”

Thus was it shown that a critical molecule involved in the circadian clock interacts directly with a protein that is known to suppressing tumour formation. This marks the first time that direct protein-protein interaction between hPer2 and tumour suppressor hp53 has been demonstrated.

The results might prove to be extremely useful in developing preventive strategies for cancer, specially for people who have disrupted sleep cycles, thereby exposing them to an increased risk of developing the disease. This would apply to those individuals working during night shifts.


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