Li Yunlong, Zhang Lisha, Yang Chunfa, Li Riheng, Shang Longbin, Zou Xiaoming
Department of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150080, P.R. China.
Department of General Surgery, The Affiliated Hospital of Hebei University, Baoding, Hebei 071000, P.R. China.
Oncol Lett. 2017 Feb;13(2):777-783. doi: 10.3892/ol.2016.5485. Epub 2016 Dec 12.
The aim of the present study was to identify the candidate genes induced by trichostatin A (TSA) in BGC-823 gastric cancer (GC) cells and to explore the possible inhibition mechanism of TSA in GC. Gene expression data were obtained through chip detection, and differentially expressed genes (DEGs) between GC cells treated with TSA and untreated GC cells (control group) were identified. Gene ontology analysis of the DEGs was performed using the database for annotation, visualization and integrated discovery. Then sub-pathway enrichment analysis was performed and a microRNA (miRNA) regulatory network was constructed. We selected 76 DEGs, among which 43 were downregulated genes and 33 were upregulated genes. By sub-pathway enrichment analysis of the DEGs, the propanoate metabolism pathway was selected as the sub-pathway. By constructing a miRNA regulatory network, we identified that and were the top hub nodes. The propanoate metabolism pathway and the genes and may play significant roles in the inhibition of GC induced by TSA. These genes may be potential therapeutic targets for GC. However, further experiments are still required to confirm our results.
本研究的目的是鉴定曲古抑菌素A（TSA）在BGC-823胃癌（GC）细胞中诱导的候选基因，并探讨TSA对GC的可能抑制机制。通过芯片检测获得基因表达数据，鉴定TSA处理的GC细胞与未处理的GC细胞（对照组）之间的差异表达基因（DEG）。使用注释、可视化和综合发现数据库对DEG进行基因本体分析。然后进行子通路富集分析并构建微小RNA（miRNA）调控网络。我们选择了76个DEG，其中43个是下调基因，33个是上调基因。通过对DEG进行子通路富集分析，选择丙酸盐代谢途径作为子通路。通过构建miRNA调控网络，我们确定 和 是顶级枢纽节点。丙酸盐代谢途径以及基因 和 可能在TSA诱导的GC抑制中发挥重要作用。这些基因可能是GC的潜在治疗靶点。然而，仍需要进一步的实验来证实我们的结果。
