Protein kinase C inhibitors suppress cell growth in established and low-passage glioma cell lines. A comparison between staurosporine and tamoxifen.
Protein kinase C inhibitors suppress cell growth in established and low-passage glioma cell lines. A comparison between staurosporine and tamoxifen.
复制标题
蛋白激酶 C 抑制剂可抑制已建立的和低传代神经胶质瘤细胞系中的细胞生长。
DOI：
10.1097/00006123-199309000-00021
复制
发表时间：
1993
期刊：
影响因子：
4.8
通讯作者：
V. Yong
中科院分区：
文献类型：
--
作者：
G. Baltuch;W. Couldwell;J. Villemure;V. Yong
We have previously demonstrated that the proliferation of established human glioma cell lines correlated with protein kinase C (PKC) activity and that a relatively selective PKC inhibitor, staurosporine, inhibits glioma cell proliferation. The purpose of this study was to determine whether low-passage glioma cell lines were also sensitive to staurosporine and to compare the antimitotic effects of staurosporine with tamoxifen, an antiestrogen with a known PKC inhibitory effect presently being investigated in the treatment of recurrent glioma. We measured the effects of treatment with staurosporine or tamoxifen on the proliferation rate of five established glioma cell lines (A172, U251, U87, U373, U563) and four low-passage glioma cell lines. The proliferation of all cell lines was inhibited by staurosporine, at an IC50 value (concentration at which activity is 50% inhibited) of approximately 2 nmol/L. All established lines, but only one low-passage line, were susceptible to tamoxifen, with an IC50 value of 10 mumol/L. Three of the four low-passage lines were poorly inhibited by tamoxifen. The IC50 values for the inhibition of cellular proliferation by staurosporine and tamoxifen closely corresponds to the IC50 data for the inhibition of particulate PKC activity in gliomas. We conclude that staurosporine is more effective in the inhibition of glioma proliferation than tamoxifen and that staurosporine is potentially useful in the adjuvant treatment of gliomas. The correspondence in IC50 results for proliferation and PKC activity further strengthens the hypothesis that an aberrant PKC system in gliomas drives their hyperproliferative state.
