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环磷酸腺苷介导的胶质瘤和神经母细胞瘤细胞鸟氨酸脱羧酶的诱导作用。

Cyclic AMP-mediated induction of ornithine decarboxylase of glioma and neuroblastoma cells.

作者信息

Bachrach U

出版信息

Proc Natl Acad Sci U S A. 1975 Aug;72(8):3087-91. doi: 10.1073/pnas.72.8.3087.

DOI:10.1073/pnas.72.8.3087
PMID:171652
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC432925/
Abstract

The activity of ornithine decarboxylase (EC 4.1.1.17; L-ornithine carboxy-lyase) of C6-BU-1 glioma and N115 neuroblastoma cells increases significantly when confluent cultures are treated with compounds that increase cellular cAMP levels. These include norepinephrine or isoproterenol, and prostaglandin E1 or adenosine, which stimulate ornithine decarboxylase activity in C6-BU-1 glioma and N115 neuroblastoma cells, respectively. Ornithine decarboxylase activity is also elevated in confluent C6-BU-1 glioma cells treated with dibutyrylcAMP and theophylline, or after the glioma cells are fed with a serum-depleted medium in the presence of catecholamines and inhibitors of cyclic nucleotide phosphodiesterase. The activity of the enzyme increases 500- to 1000-fold, 2-6 hr after stationary-phase N115 neuroblastoma cells are fed with a serum-free medium, supplemented with phosphodiesterase inhibitors, adenosine, or prostaglandin E1. This stimulation is antagonized by carbamoyl choline and is blocked by actinomycin D or cycloheximide. These results suggest that the synthesis of ornithine decarboxylase of C6-BU-1 glioma and N115 neuroblastoma cells is controlled by cAMP.

摘要

当汇合培养的C6 - BU - 1胶质瘤细胞和N115神经母细胞瘤细胞用能提高细胞cAMP水平的化合物处理时,鸟氨酸脱羧酶(EC 4.1.1.17;L - 鸟氨酸羧基裂解酶)的活性显著增加。这些化合物包括去甲肾上腺素或异丙肾上腺素,以及前列腺素E1或腺苷,它们分别刺激C6 - BU - 1胶质瘤细胞和N115神经母细胞瘤细胞中的鸟氨酸脱羧酶活性。用二丁酰cAMP和茶碱处理汇合的C6 - BU - 1胶质瘤细胞时,或者在胶质瘤细胞在儿茶酚胺和环核苷酸磷酸二酯酶抑制剂存在的情况下用无血清培养基培养后,鸟氨酸脱羧酶活性也会升高。当静止期的N115神经母细胞瘤细胞用补充了磷酸二酯酶抑制剂、腺苷或前列腺素E1的无血清培养基培养时,该酶的活性在2 - 6小时后增加500 - 1000倍。这种刺激作用被氨甲酰胆碱拮抗,并被放线菌素D或环己酰亚胺阻断。这些结果表明,C6 - BU - 1胶质瘤细胞和N115神经母细胞瘤细胞中鸟氨酸脱羧酶的合成受cAMP控制。

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