Microarray gene expression profiling reveals potential mechanisms of tumor suppression by the class I HDAC-selective benzoylhydrazide inhibitors.
Microarray gene expression profiling reveals potential mechanisms of tumor suppression by the class I HDAC-selective benzoylhydrazide inhibitors.
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DOI：
10.1016/j.gdata.2015.06.019
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发表时间：
2015-09-01
期刊：
影响因子：
--
通讯作者：
Liao D
中科院分区：
文献类型：
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作者：
Mahmud I;Liao D
组蛋白去乙酰化酶（HDAC）抑制剂（HDIs）具有治疗癌症和其他疾病的治疗潜力。HDIs对基因表达的调节是其治疗作用的主要机制。通过高通量筛选活动发现了一类具有先前未描述的苯甲酰肼支架的新型HDI。使用基因表达的微阵列分析，我们以前已经证明，治疗乳腺癌细胞与铅苯甲酰肼HDI UF010的结果在细胞周期阻滞和凋亡，可能通过激活肿瘤抑制途径与致癌途径的同时抑制。在这份简短的报告中，我们展示了方法和分析细节，并讨论了其他途径，如受UF010影响的免疫信号传导。将来自微阵列的原始和处理的数据以登录号GSE 56823保藏在NCBI的基因表达综合数据库（GEO）中。
Histone deacetylase (HDAC) inhibitors (HDIs) have therapeutic potentials for treating cancer and other diseases. Modulation of gene expression by HDIs is a major mechanism underlying their therapeutic effects. A novel class of HDIs with a previously undescribed benzoylhydrazide scaffold has been discovered through a high throughput screening campaign. Using microarray profiling of gene expression, we have previously demonstrated that treatment of breast cancer cells with a lead benzoylhydrazide HDI UF010 results in cell cycle arrest and apoptosis, likely through activation of tumor suppression pathways with concurrent inhibition of oncogenic pathways. In this brief report, we show methodological and analytical details and discuss additional pathways such as immune signaling that are affected by UF010. Raw and processed data from the microarray were deposited in NCBI's Gene Expression Omnibus (GEO) database under the accession number: GSE56823.