Rapamycin-induced G1 arrest in cycling B-CLL cells is associated with reduced expression of cyclin D3, cyclin E, cyclin A, and survivin.

摘要: In B-cell chronic lymphocytic leukemia (B-CLL), malignant cells seem to be arrested in the G(0)/early G(1) phase of cell cycle, and defective apoptosis might involved disease progression. However, increasing evidence exists that B-CLL is more than a consisting slowly accumulating resting B cells: proliferating pool has been described lymph nodes bone marrow feed blood. Rapamycin reported inhibit cycle progression variety types, including human cells, shown activity against broad range tumor lines. Therefore, we investigated ability rapamycin block cells. We have recently demonstrated stimulation with CpG-oligonucleotides interleukin-2 provides valuable model for studying regulation our present study, induced arrest inhibited phosphorylation p70s6 kinase (p70(s6k)). contrast previous reports on nonmalignant expression inhibitor p27 was not changed rapamycin-treated leukemic Treatment prevented retinoblastoma protein (RB) without affecting cyclin D2, but D3 no longer detectable addition, treatment cyclin-dependent 2 by preventing up-regulation E A. Interestingly, survivin, which expressed proliferation centers patients vivo, up-regulated interferes many critical molecules cycling conclude from study an attractive substance therapy inducing