Smirnov A S, Ruzov A S, Budanov A V, Prokhortchouk A V, Ivanov A V, Prokhortchouk E B
Group of Transcriptional Control and Oncogenesis, Institute of Gene Biology, Russian Academy of Sciences, Vavilova 34/5, 117334 Moscow, Russia.
Cell Death Differ. 2001 Jun;8(6):621-30. doi: 10.1038/sj.cdd.4400853.
Most of cells exhibit low nuclear level of NF-kappaB. However, in some cell lines and tissues aberrantly activated NF-kappaB is playing an important role in cell motility, growth control and survival. Here we describe the result of decrease of constitutive NF-kappaB level in different adenocarcinoma cell lines. Treatment of mouse adenocarcinoma cell line CSML-100 with both synthetic (TPCK or PDTC) or natural (I(kappaB)-alpha) NF-kappaB inhibitors caused apoptotic death. Low doses of TPCK were harmless for CSML100 cells but sensitized them to TNF-induced apoptosis. Death of CSML100 cells in the presence of high concentration TPCK was not accompanied with significant changes in c-myc activity but strongly correlated with rapid decrease in p53 level. Thus, mutual behavior p53 and NF-kappaB represented a unique feature of TPCK-induced apoptosis in CSML-100 adenocarcinoma cells.
大多数细胞中NF-κB的核水平较低。然而，在一些细胞系和组织中，异常激活的NF-κB在细胞运动、生长控制和存活中发挥着重要作用。在此，我们描述了不同腺癌细胞系中组成型NF-κB水平降低的结果。用合成（TPCK或PDTC）或天然（IκB-α）NF-κB抑制剂处理小鼠腺癌细胞系CSML-100会导致凋亡死亡。低剂量的TPCK对CSML100细胞无害，但会使它们对TNF诱导的凋亡敏感。高浓度TPCK存在时CSML100细胞的死亡与c-myc活性的显著变化无关，但与p53水平的快速降低密切相关。因此，p53和NF-κB的相互作用表现为TPCK诱导CSML-100腺癌细胞凋亡的一个独特特征。
