RB pockets the cell cycle

Widely used cancer therapies inflict collateral damage on normal dividing cells. But now Lohez et al. (page 67) find a way to distinguish normally cycling cells from cancer cells using actin inhibitors that cause an RB-dependent cell cycle arrest.

High levels of actin inhibitors prevent cell cleavage and thus lead to a doubling of cellular DNA and subsequent cell death. However, cells usually sense the problem and halt the cell cycle in G1.

The authors found that very low levels of actin inhibitors that do not affect most cellular processes still induce a reversible G1 arrest. This sensitive response requires the function of RB pocket proteins (RB, p107, and p130) but is independent of p53.

The arrest may arise because the drug-treated cells believe that they...