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首页> 外文期刊>Lung cancer: Journal of the International Association for the Study of Lung Cancer >Downregulation of Sirt1 by antisense oligonucleotides induces apoptosis and enhances radiation sensitization in A549 lung cancer cells.
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Downregulation of Sirt1 by antisense oligonucleotides induces apoptosis and enhances radiation sensitization in A549 lung cancer cells.

机译：Downregulation Sirt1的反义寡核苷酸诱导细胞凋亡和增强辐射敏感A549肺癌细胞。

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摘要

Sirt1, a conserved nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase, has been implicated in modulating transcriptional silencing and cell survival, and seems to play a key role in carcinogenesis through deacetylation of important regulatory proteins. This makes it a potential target in cancer therapy. The purpose of this study was to determine whether inhibition of Sirt1 by using antisense oligonucleotides (ASODN) induces apoptosis and enhances radiation sensitization in A549 lung cancer cells. Initially, transient transfection of A549 lung cancer cells with ASODN against Sirt1 specifically reduced Sirt1 expression in a dose-dependent and sequence-specific manner, at both mRNA and proteins levels. The inhibition of Sirt1 obviously decreased A549 cells survival, induced G1 arrest as well as apoptosis. Furthermore, the inhibition of Sirt1 by ASODN greatly increased radiation-induced antiproliferation effects involving in increasing acetylation of tumour suppressor p53 and Bax expression in A549 lung cancer cells. In summary, our results indicate that downregulation of Sirt1 by ASODN decreases survival and increases radiation-induced antiproliferation effects of human lung cancer cells and suggest that inhibition of Sirt1 by ASODN may be a potential gene therapy approach to the treatment of lung cancer.
机译：Sirt1,守恒的烟酰胺腺嘌呤二核苷酸(NAD(+))端依赖脱乙酰酶参与调节转录沉默和细胞生存和发挥通过脱乙酰作用关键作用在致癌作用重要的调控蛋白。在癌症治疗的潜在目标。本研究旨在确定是否抑制使用反义寡核苷酸Sirt1的(ASODN)凋亡和增强辐射在A549肺癌细胞致敏。最初,瞬时转染的A549肺肿瘤细胞与ASODN Sirt1在一个特别减少了Sirt1表达式sequence-specific方式,存在剂量依赖的相关性信使rna和蛋白质的水平。显然Sirt1 A549细胞存活率降低,诱导G1逮捕以及细胞凋亡。此外,ASODN Sirt1的抑制大大增加辐射诱导抗涉及增加的影响乙酰化作用的肿瘤抑制基因p53和伯灵顿在A549肺癌细胞表达。Sirt1的差别我们的研究结果表明,对这些基因由ASODN增加生存和减少辐射诱导抗的影响人类肺癌细胞和建议抑制由ASODN Sirt1可能是潜在的基因治疗肺癌的治疗方法癌症。

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