Scott R E, Gao S
Department of Pathology, University of Tennessee Health Science Center, 3 North Dunlap Street, Memphis, TN 38163, USA.
Anticancer Res. 2002 Nov-Dec;22(6C):3837-42.
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.
细胞从G1期经S期到有丝分裂的进程可受微管依赖性机制影响，这些机制涉及AP1因子和c-Jun氨基末端激酶（JNK）活性。紫外线照射诱导的细胞凋亡也涉及AP1因子和JNK活性。当前研究评估了P2P-R缺乏对这些机制的影响，因为在分化过程中，P2P-R表达与AP1诱导性降低及细胞周期进程相关联而受到抑制，且P2P-R过表达会促进细胞凋亡。
在天然细胞与经P2P-R反义处理而P2P-R缺乏的细胞中，评估微管破坏药物诺考达唑诱导有丝分裂停滞的能力以及紫外线照射诱导细胞凋亡的能力。
P2P-R缺乏以微管依赖性方式限制细胞从G1期经S期到有丝分裂的进程，且P2P-R缺乏会抑制紫外线照射诱导的细胞凋亡。
P2P-R可能影响AP1和/或JNK信号通路。
