Multiple pathways are involved in protection of MCF‐7 cells against death due to protein synthesis inhibition
Multiple pathways are involved in protection of MCF‐7 cells against death due to protein synthesis inhibition
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多种途径参与保护 MCF-7 细胞免于因蛋白质合成抑制而死亡
DOI：
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发表时间：
1995
影响因子：
5.6
通讯作者：
A. Karasik
中科院分区：
文献类型：
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作者：
A. Geier;Chana Weiss;R. Beery;M. Haimsohn;R. Hemi;Z. Malik;A. Karasik
此前，我们已经证明IGF-1保护MCF-7细胞免受蛋白质合成抑制剂放线菌酮(CHX)诱导的死亡。在本研究中，我们研究了蛋白激酶C激活剂12-0-十四酰佛波醇-13-乙酸酯(TPA)、蛋白激酶A激活剂8-溴腺苷3‘5’-环一磷酸(BR-cAMP)和酶抑制剂金曲酸(ATA)保护MCF-7细胞免受CHX持续存在的死亡的能力。孵育48h后，用台盼蓝染色、乳酸脱氢酶释放、细胞三磷酸腺苷含量、透射电子显微镜和DNA片段化等方法检测细胞死亡情况。以坏死为终点的细胞凋亡是这种细胞死亡方式的特征。最适浓度分别为40 ng/ml和100μg/ml的TPA和ATA可将细胞死亡降低至对照水平(不含CHX)，而最佳浓度为650μg/ml的BrcAMP仅部分减少细胞死亡。刺激对照MCF-7细胞蛋白质合成的IGF-1、TPA和ATA对CHX处理细胞的蛋白质合成没有影响，表明存活效应不是由于新的蛋白质合成所致。蛋白激酶C抑制剂星形孢子素以剂量依赖方式阻断TPA和IGF-1的存活效应，但不影响ATA的存活效应。酪氨酸激酶抑制剂金雀异黄素可阻断IGF-1的存活效应，但不能阻断TPA和ATA的存活效应。我们的结果为几个不同的通路提供了证据，这些通路的激活通过抑制蛋白质合成来保护MCF-7细胞免于死亡。©1995 Wiley-Liss公司
Previously we have shown that IGF‐1 protected MCF‐7 cells against death induced by the protein synthesis inhibitor cycloheximide (CHX). In the present study we investigated the ability of protein kinase C activator 12‐0‐tetradecanoyl‐phorbol‐13‐acetate (TPA), the protein kinase A activator 8‐bromoadenosine 3′5′‐cyclic monophosphate (Br‐cAMP), and the enzyme inhibitor aurintricarboxylic acid (ATA) to protect MCF‐7 cells against death, due to a continuous presence of CHX. Cell death was evaluated after 48 h of incubation by several techniques (trypan blue staining, release of lactic dehydrogenase, cellular ATP content, transmission electron microscopy, and DNA fragmentation). Apoptosis which terminates in necrosis, characterized this mode of cell death. TPA and ATA at optimal concentrations of 40 ng/ml and 100 μg/ml, respectively, reduced cell death to the control level (without CHX), while Br‐cAMP at an optimal concentration of 650 μg/ml reduced cell death only partially. IGF‐1, TPA, and ATA, which stimulated protein synthesis in the control MCF‐7 cells, had no effect on protein synthesis in the CHX‐treated cells, indicating that the survival effect is not due to new protein synthesis. The protein kinase C inhibitor staurosporine blocked the survival effect of TPA and IGF‐1 in a dose‐dependent manner, however did not affect the survival effect of ATA. The tyrosine kinase inhibitor genistein blocked the survival effect of IGF‐1, but not that of TPA and ATA. Our results provide evidence for several distinctive pathways, the activation of which protects MCF‐7 cells against death, due to protein synthesis inhibition. © 1995 Wiley‐Liss, Inc.
酸性和碱性成纤维细胞生长因子是在静止的 BALB/c 3T3 小鼠成纤维细胞中具有独特活性的存活因子。
DOI：
10.1073/pnas.88.8.3372
发表时间：
1991
影响因子：
11.1
作者：
Tamm,I;Kikuchi,T;Zychlinsky,A
通讯作者：
Zychlinsky,A
糖皮质激素组织特异性诱导核小体间脱氧核糖核酸裂解活性和细胞凋亡的机制。
影响因子：
4.8
作者：
Schwartzman,RA;Cidlowski,JA
通讯作者：
Cidlowski,JA
Madin-Darby 犬肾细胞中胰岛素样生长因子介导的磷酸化和原癌基因诱导。
DOI：
10.1210/mend-5-1-51
发表时间：
1991
期刊：
Molecular endocrinology (Baltimore, Md.)
影响因子：
--
作者：
Hauguel-deMouzon,S;Kahn,CR
通讯作者：
Kahn,CR