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通过非诱变浓度的5-氮杂胞苷诱导癌变过程中的一个步骤,该步骤通常与诱变作用相关。

Induction of a step in carcinogenesis that is normally associated with mutagenesis by nonmutagenic concentrations of 5-azacytidine.

作者信息

Bouck N, Kokkinakis D, Ostrowsky J

出版信息

Mol Cell Biol. 1984 Jul;4(7):1231-7. doi: 10.1128/mcb.4.7.1231-1237.1984.

DOI:10.1128/mcb.4.7.1231-1237.1984
PMID:6209558
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC368903/
Abstract

The permanent cell line BHK-21/cl 13 can be transformed by mutagenic carcinogens as the result of the induction of a recessive somatic mutation. Yet when these cells were treated with 5-azacytidine under conditions in which no mutants resistant to either ouabain or 6-thioguanine could be detected, they were transformed efficiently. These transformants were induced, not selected. 6-Azacytidine was ineffective at transforming BHK cells; 2'-deoxy-5-azacytidine was exceptionally effective. When tested by cell fusion, transformants induced by 5-azacytidine fell into the same complementation group as those induced by highly mutagenic carcinogens, but they were phenotypically distinct in that they were unstable during prolonged passage and rarely displayed the temperature-limited phenotypes so common among BHK transformants induced by strongly mutagenic carcinogens. These results raise the possibility that a cell can be induced by either genetic or epigenetic means to traverse the same single step in carcinogenesis.

摘要

永久性细胞系BHK-21/cl 13可因隐性体细胞突变的诱导而被诱变致癌物转化。然而,当这些细胞在无法检测到对哇巴因或6-硫鸟嘌呤耐药的突变体的条件下用5-氮杂胞苷处理时,它们被有效地转化了。这些转化体是诱导产生的,而非筛选出来的。6-氮杂胞苷对BHK细胞的转化无效;2'-脱氧-5-氮杂胞苷则异常有效。通过细胞融合试验检测时,5-氮杂胞苷诱导的转化体与高诱变致癌物诱导的转化体属于同一互补群,但它们在表型上有所不同,即它们在长时间传代过程中不稳定,并且很少表现出在强诱变致癌物诱导的BHK转化体中常见的温度限制表型。这些结果增加了一种可能性,即细胞可以通过遗传或表观遗传方式被诱导在致癌过程中跨越相同的单一阶段。

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Induction of a step in carcinogenesis that is normally associated with mutagenesis by nonmutagenic concentrations of 5-azacytidine.通过非诱变浓度的5-氮杂胞苷诱导癌变过程中的一个步骤,该步骤通常与诱变作用相关。
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引用本文的文献

1
The majority of independently transformed BHK cell clones share a single functional lesion which determines anchorage independence and influences tumorigenicity.大多数独立转化的BHK细胞克隆具有单一的功能性损伤,这种损伤决定了锚定非依赖性并影响致瘤性。
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2
Differential activation of the hprt gene on the inactive X chromosome in primary and transformed Chinese hamster cells.原代和转化的中国仓鼠细胞中失活X染色体上hprt基因的差异激活。
Mol Cell Biol. 1989 Apr;9(4):1635-41. doi: 10.1128/mcb.9.4.1635-1641.1989.
3
Sudden outbreak of a leukemia-like lesion in female CBA mice after repeated injections of 5-azacytidine.在雌性CBA小鼠反复注射5-氮杂胞苷后,突然爆发了一种类似白血病的病变。
J Cancer Res Clin Oncol. 1988;114(5):525-7. doi: 10.1007/BF00391506.
4
Capture and characterization of 5-aza-2'-deoxycytidine-treated C3H/10T1/2 cells prior to transformation.转化前对经5-氮杂-2'-脱氧胞苷处理的C3H/10T1/2细胞的捕获与鉴定。
Proc Natl Acad Sci U S A. 1988 Sep;85(17):6384-8. doi: 10.1073/pnas.85.17.6384.
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Carcinogenicity and haemoglobin synthesis induction by cytidine analogues.胞苷类似物的致癌性及血红蛋白合成诱导作用
Br J Cancer. 1988 Apr;57(4):395-402. doi: 10.1038/bjc.1988.89.
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Clonal analysis of the malignant properties of B16 melanoma cells treated with the DNA hypomethylating agent 5-azacytidine.用DNA低甲基化剂5-氮杂胞苷处理的B16黑色素瘤细胞恶性特性的克隆分析
Clin Exp Metastasis. 1988 May-Jun;6(3):185-200. doi: 10.1007/BF01782479.
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Interferon-induced revertants of ras-transformed cells: resistance to transformation by specific oncogenes and retransformation by 5-azacytidine.干扰素诱导的ras转化细胞回复突变体:对特定癌基因转化的抗性及5-氮杂胞苷的再转化作用
Mol Cell Biol. 1987 Jun;7(6):2196-200. doi: 10.1128/mcb.7.6.2196-2200.1987.
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Effects of 5-azacytidine on the progressive nature of cell transformation.5-氮杂胞苷对细胞转化进展特性的影响。
Mol Cell Biol. 1985 Jul;5(7):1800-3. doi: 10.1128/mcb.5.7.1800-1803.1985.
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5-Azacytidine and RNA secondary structure increase the retrovirus mutation rate.5-氮杂胞苷和RNA二级结构可提高逆转录病毒的突变率。
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