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Novel connection found between biological clock and cancer

in mammals checkpoint kinase-2 (CHK2), whose normal role is exclusively in regulating the cell division cycle. CHK2 physically interacts with FRQ; the mutation makes this interaction much stronger. However, a mutant enzyme that has lost its activity has no effect on the clock.

Normally CHK2 is involved in the signal response pathway that begins when DNA is damaged and results in a temporary stoppage of cell division until the damage is fixed. The researchers found that the resetting effect of DNA damage requires the period-4 clock protein, and that period-4 is the homolog, the Neurospora version, of the mammalian checkpoint kinase.

Moreover, the clock regulates expression of the period-4 gene. This closes a loop connecting the clock to period-4 and period-4 to the clock and the cell cycle. The clock normally modulates expression of this gene that encodes an important cell cycle regulator, and that cell cycle regulator in turn affects not only the cell cycle but also the clock.

Recent evidence in mammalian cells shows that other cell cycle regulators physically interact with clock proteins. Loss of at least one clock protein (mammalian period-2) is known to increase cancer susceptibility. The coordination of the clock and cell division through cell cycle checkpoints, supports the clock's "integral role in basic cell biology," conclude the researchers." Their work can help advance understanding of cancer origins as well as the timing of anti-cancer treatment.


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Source:Dartmouth Medical School


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