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在17种分化诱导剂中,只有丁酸钠能使伯基特淋巴瘤中的c-myc永久下调。

Among 17 inducers of differentiation only sodium butyrate causes a permanent down-regulation of c-myc in Burkitt's lymphoma.

作者信息

Rottleb C, Bornkamm G W, Polack A

机构信息

Krankenhaus München Bogenhausen, Munich, Germany.

出版信息

Int J Cancer. 1995 Sep 15;62(6):697-702. doi: 10.1002/ijc.2910620609.

Abstract

De-regulation of c-myc by chromosomal translocation is one crucial step for the development of Burkitt's lymphoma. The de-regulation is caused through juxtaposition of c-myc with one of the 3 immunoglobulin loci. We have reported earlier that treatment of Burkitt's lymphoma cells with n-butyrate causes transcriptional down-regulation of c-myc expression. Because of the possible therapeutic implication of this result, we looked for other compounds which, on the one hand, might be applicable in vivo and, on the other hand, might cause down-regulation of c-myc expression in Burkitt's lymphoma cells. Since n-butyrate is known to induce differentiation, we have examined other differentiation inducers of different chemical nature for their ability to reduce c-myc expression in Burkitt's lymphoma cells. Many of the substances tested caused down-regulation of c-myc expression, which, however, was transient except for n-butyrate. Three types of compounds proved to be particularly active: polar planar compounds (e.g., dimethylsulfoxide), heterocyclic compounds (e.g., hypoxanthine), and short-chain fatty acids (e.g., n-butyric acid). The action of n-butyrate on c-myc suppression was exceptional not only in not being transient, but also in being allele-specific: it down-regulated the translocated allele without affecting the normal one. Medium transfer experiments revealed that neither degradation of the active compound nor an intracellular resistance mechanism can fully account for the reversibility of c-myc down-regulation after treatment with the transiently acting polar planar compounds.

摘要

染色体易位导致的c-myc失调是伯基特淋巴瘤发生发展的关键步骤。这种失调是由于c-myc与3个免疫球蛋白基因座之一并列所致。我们之前报道过,用正丁酸盐处理伯基特淋巴瘤细胞会导致c-myc表达的转录下调。鉴于这一结果可能具有的治疗意义,我们寻找了其他化合物,一方面这些化合物可能适用于体内,另一方面可能导致伯基特淋巴瘤细胞中c-myc表达下调。由于已知正丁酸盐可诱导分化,我们研究了其他不同化学性质的分化诱导剂降低伯基特淋巴瘤细胞中c-myc表达的能力。许多测试物质都导致了c-myc表达的下调,但除正丁酸盐外,这种下调都是短暂的。有三类化合物被证明特别有效:极性平面化合物(如二甲基亚砜)、杂环化合物(如次黄嘌呤)和短链脂肪酸(如正丁酸)。正丁酸盐对c-myc抑制的作用不仅在不具有短暂性方面是例外,而且在等位基因特异性方面也是例外:它下调易位等位基因而不影响正常等位基因。培养基转移实验表明,活性化合物的降解和细胞内抗性机制都不能完全解释用短暂作用的极性平面化合物处理后c-myc下调的可逆性。

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