胰岛素对人恶性胶质瘤蛋白磷酸化和蛋白激酶C活性的影响。

B C Yang, R F Chen, C C Chio, W C Chang, M T Lin, S J Lin
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引用次数: 0

摘要

研究了胰岛素对胶质瘤和正常胶质细胞中蛋白磷酸化活性的调节作用。胰岛素以剂量依赖的方式抑制胶质瘤细胞的体外蛋白磷酸化,同时刺激脑膜瘤、神经鞘瘤和胶质细胞的磷酸化。尽管胶质瘤和神经胶质细胞在治疗前含有不同种类的酪氨酸磷酸化蛋白,但它们对胰岛素的反应表达了相似种类的酪氨酸磷酸化蛋白。胰岛素增加了胶质瘤和正常胶质细胞中酪蛋白激酶II和总蛋白激酶C (PKC)的活性。胰岛素可提高U373-MG细胞的PKC活性。PKC同工酶,包括α、β、δ、epsilon和γ亚型,在胶质瘤中检测到,但在胶质细胞中很少发现。胰岛素下调胶质瘤中胞浆pkc - γ和膜结合PKC-epsilon蛋白。这些结果表明,在人类胶质瘤中存在胰岛素信号通路的改变,这可能涉及PKC同工酶的差异调节。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of insulin on protein phosphorylation and protein kinase C activity in human malignant gliomas.

Modulation of protein phosphorylation activities by insulin was investigated in glioma and normal glial cells. Insulin suppressed the in vitro protein phosphorylation of glioma cells in a dose-dependent manner while it stimulated that of meningiomas, neurilemmomas and glial cells. Although gliomas and glial cells contained different species of tyrosyl phosphoproteins before treatment, they expressed similar kinds of tyrosyl phosphoproteins in response to insulin. Insulin increased the activities of casein kinase II and total protein kinase C (PKC) in glioma and normal glial cells. The membrane-bound PKC activity in U373-MG cells was elevated by insulin. The PKC isozymes, including subtypes alpha, beta, delta, epsilon and gamma, were detected in gliomas, but few were found in glial cells. Insulin down regulated the cytosolic PKC-gamma and the membrane-bound PKC-epsilon proteins in gliomas. These results indicate that an altered insulin signaling pathway exists in human gliomas, which might involve differential regulation of PKC isozymes.

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