Figure 8.

A schematic model of how p53 via activation of miR-26a and miR-16 promotes G1/S arrest and apoptosis in response to genotoxic drugs. On the one hand, miR-16 and 26a downregulate G2/M checkpoint kinases, Chk1 and Wee1, resulting in slippage of damaged cancer cells from the mitotic checkpoint arrest and their elimination via apoptosis. On the other hand, miR-16 represses expression of several cell cycle promoting genes, including cyclin E, cyclin D, cdk4 and cdk6 resulting in their arrest in G1/S, which subsequently elicits apoptosis