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首页> 外文期刊>Pathobiology: journal of immunopathology, molecular and cellular biology >Protein kinase C-mediated in vitro invasion of human glioma cells through extracellular-signal-regulated kinase and ornithine decarboxylase.
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Protein kinase C-mediated in vitro invasion of human glioma cells through extracellular-signal-regulated kinase and ornithine decarboxylase.

机译：蛋白激酶C通过细胞外信号调节激酶和鸟氨酸脱羧酶介导的人脑胶质瘤细胞的体外侵袭。

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摘要

We investigated the involvement of protein kinase C (PKC) in the in vitro invasiveness of the A-172, U-87 and U-373 human glioma cell lines, as well as the role of ornithine decarboxylase (ODC) and/or extracellular-signal-regulated kinase (ERK) in the actions of PKC. Thus, cells were treated under serum-free conditions with the PKC activator phorbol 12-myristate 13-acetate (PMA), or with the PKC inhibitors bisindolylmaleimide I (GF 109203X) or calphostin C in the absence or presence of the ODC inhibitor D,L-alpha-difluoromethylornithine (DFMO), and/or the mitogen-activated protein kinase/extracellular-signal-regulated kinase inhibitor 2'-amino-3'-methoxyflavone (PD 098059). Subsequently, cells were assessed for membrane-type 1 matrix metalloproteinase (MT1-MMP) mRNA contents, 72-kD latent, and 59/62-kD activated matrix metalloproteinase 2 (MMP-2) in conditioned media, as well as invasiveness. For these purposes, we used Northern blot analysis, gelatine zymography, and an in vitro filter invasion assay, respectively. Data were related to those found with untreated cells. PKC activity was 2- to 3-fold stimulated by PMA (100 nM for 30 min), and about 2-fold inhibited by calphostin C (40 nM for 2 h) or GF 109203X (5 microM for 20 min). This was accompanied by a similar increase or decrease, respectively, in MT1-MMP mRNA expression, 59/62-kD MMP-2 activity, and in vitro invasion. Inhibition of ODC activity (about 2-fold by 24 h DFMO 5 mM), ERK activation (almost completely by 20 min PD 098059 50 microM), or both these enzymes simultaneously led to a reduction by about half in levels of MT1-MMP mRNA, 59/62-kD MMP-2 activity, and invasion in untreated as well as PMA-stimulated cells. The use of these compounds did not significantly alter the inhibitory effects of GF 109203X or calphostin C. Modulation of PKC and/or ERK activity resulted in corresponding changes in ERK and/or ODC activities, but interference with ODC affected neither ERK nor PKC. Our data suggest a regulatory role for PKC, in co-operation with ERK and ODC, in glioma cell invasion, by modulation of MT1-MMP mRNA expression and MMP-2 activation. Copyright 2001 S. Karger AG, Basel
机译：我们调查了蛋白激酶C（PKC）在A-172，U-87和U-373人神经胶质瘤细胞系的体外侵袭中的作用，以及鸟氨酸脱羧酶（ODC）和/或细胞外蛋白的作用PKC作用中的信号调节激酶（ERK）。因此，在无血清条件下，在无或有ODC抑制剂D的情况下，用PKC激活剂佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）或PKC抑制剂比辛多尔基马来酰亚胺I（GF 109203X）或钙磷蛋白C处理细胞。 L-α-二氟甲基鸟氨酸（DFMO）和/或促分裂原活化的蛋白激酶/细胞外信号调节的激酶抑制剂2'-氨基-3'-甲氧基黄酮（PD 098059）。随后，评估细胞在条件培养基中的膜型1基质金属蛋白酶（MT1-MMP）mRNA含量，72 kD潜伏性和59/62 kD活化基质金属蛋白酶2（MMP-2）的侵袭性。为了这些目的，我们分别使用了RNA印迹分析，明胶酶谱分析和体外滤膜侵袭试验。数据与未经处理的细胞发现的数据有关。 PKC活性被PMA（100 nM，持续30分钟）刺激了2至3倍，而钙磷蛋白C（40 nM，持续2小时）或GF 109203X（5 microM，20分钟）抑制了约2倍。分别伴随着MT1-MMP mRNA表达，59 / 62-kD MMP-2活性和体外侵袭的相似增加或减少。抑制ODC活性（约24小时DFMO 5 mM的2倍），ERK激活（20分钟PD 098059 50 microM几乎完全）或这两种酶同时导致MT1-MMP mRNA水平降低约一半，59 / 62-kD MMP-2活性以及在未处理以及PMA刺激的细胞中的侵袭。这些化合物的使用不会显着改变GF 109203X或钙磷蛋白C的抑制作用。PKC和/或ERK活性的调节导致ERK和/或ODC活性的相应变化，但对ODC的干扰既不会影响ERK也不会影响PKC。我们的数据表明，通过调节MT1-MMP mRNA表达和MMP-2激活，PKC在与ERK和ODC的合作中对神经胶质瘤细胞的侵袭具有调节作用。版权所有2001 S. Karger AG，巴塞尔

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