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首页> 外文期刊>BMC Medical Genomics >Transcriptomic signature of Bexarotene (Rexinoid LGD1069) on mammary gland from three transgenic mouse mammary cancer models
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Transcriptomic signature of Bexarotene (Rexinoid LGD1069) on mammary gland from three transgenic mouse mammary cancer models

机译：贝沙罗丁（Rexinoid LGD1069）在三种转基因小鼠乳癌模型中的乳腺上的转录组学特征

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Background The rexinoid bexarotene (LGD1069, Targretin) is a highly selective retinoid × receptor (RXR) agonist that inhibits the growth of pre-malignant and malignant breast cells. Bexarotene was shown to suppress the development of breast cancer in transgenic mice models without side effects. The chemopreventive effects of bexarotene are due to transcriptional modulation of cell proliferation, differentiation and apoptosis. Our goal in the present study was to obtain a profile of the genes modulated by bexarotene on mammary gland from three transgenic mouse mammary cancer models in an effort to elucidate its molecular mechanism of action and for the identification of biomarkers of effectiveness. Methods Serial analysis of gene expression (SAGE) was employed to profile the transcriptome of p53-null, MMTV-ErbB2, and C3(1)-SV40 mammary cells obtained from mice treated with bexarotene and their corresponding controls. Results This resulted in a dataset of approximately 360,000 transcript tags representing over 20,000 mRNAs from a total of 6 different SAGE libraries. Analysis of gene expression changes induced by bexarotene in mammary gland revealed that 89 genes were dysregulated among the three transgenic mouse mammary models. From these, 9 genes were common to the three models studied. Conclusion Analysis of the indicated core of transcripts and protein-protein interactions of this commonly modulated genes indicate two functional modules significantly affected by rexinoid bexarotene related to protein biosynthesis and bioenergetics signatures, in addition to the targeting of cancer-causing genes related with cell proliferation, differentiation and apoptosis.
机译：背景技术类比索罗汀（LGD1069，Targretin）是一种高度选择性的类视色素×受体（RXR）激动剂，可抑制恶性前期和恶性乳腺癌细胞的生长。证明了倍他罗汀可以在无副作用的转基因小鼠模型中抑制乳腺癌的发展。贝沙罗汀的化学预防作用归因于细胞增殖，分化和凋亡的转录调控。我们在本研究中的目标是从三种转基因小鼠乳癌模型中获得贝沙罗汀在乳腺上调节的基因的概况，以阐明其作用的分子机制并鉴定有效性的生物标志物。方法采用基因表达的序列分析（SAGE）对从贝沙罗汀治疗的小鼠及其相应对照组获得的p53-null，MMTV-ErbB2和C3（1）-SV40乳腺细胞的转录组进行分析。结果这产生了来自总共6个不同SAGE文库的大约360,000个转录物标签的数据集，代表超过20,000个mRNA。贝沙罗汀在乳腺中诱导的基因表达变化分析表明，在三种转基因小鼠乳腺模型中，有89个基因表达失调。从这些数据中，三个模型共有9个基因。结论：分析了转录本的指示核心和该共同调控基因的蛋白质-蛋白质相互作用，结果表明，除了针对与细胞增殖有关的致癌基因外，还受到了与蛋白质生物合成和生物能学特征相关的类雷诺贝沙罗汀显着影响的两个功能模块，分化和凋亡。

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