P2P-R deficiency modifies nocodazole-induced mitotic arrest and UV-induced apoptosis

Cell cycle progression from G1 through S to mitosis can be influenced by microtubule-dependent mechanisms that involve AP1 factors and c-Jun N-terminal kinase (JNK) activity. UV irradiation-induced apoptosis also involves AP1 factors and JNK activity. The current studies evaluated the outcome of P2P-R deficiency on these mechanisms because P2P-R expression is repressed in association with a decrease in AP1 inducibility and cell cycle progression during differentiation, and P2P-R overexpression promotes apoptosis.

The ability of the microtubule disruption drug nocodazole to induce mitotic arrest and the ability of UV irradiation to induce apoptosis was evaluated in native versus cells made P2P-R deficient by P2P-R antisense treatment.

P2P-R deficiency restricts cell cycle progression from G1 through S to mitosis in a microtubule-dependent manner and P2P-R deficiency represses UV irradiation-induced apoptosis.

P2P-R may influence AP1 and/or JNK signaling pathways.