Department of Gastroenterology, Zhongnan Hospital of Wuhan University, Hubei Clinical Center and Key Laboratory of Intestinal and Colorectal Diseases, Wuhan, Hubei 430071, P.R. China.
Mol Med Rep. 2017 Nov;16(5):7479-7489. doi: 10.3892/mmr.2017.7509. Epub 2017 Sep 18.
Ulcerative colitis (UC) is a chronic inflammatory bowel disease that is associated with both genetic and environmental factors; however, the underlying pathogenesis of UC remains unclear. The present study aimed to further explore 12 microarray datasets from patients with UC obtained from the Gene Expression Omnibus repository, for potential genetic pathogenesis of UC through a global bioinformatics view, which included identification of differentially expressed genes (DEGs), functional enrichments, protein‑protein interactions, transcriptional and post‑transcriptional regulation and drug‑gene associations. This integrated analysis screened 233 DEGs that were compared between UC and normal control tissue samples; these included 173 upregulated and 60 downregulated DEGs. Subsequently, transcription factors, such as TATA‑binding protein 1 (TBP1; hsa_TATAAA_V$TATA_01) and nuclear factor-κB (NF-κB; hsa_V$NFKAPPAB_01) and microRNAs (miRNAs; such as miR‑516‑3p and miR‑23a) were revealed to be associated with 233 DEGs. Notably, further analysis indicated that these DEGs were enriched in certain diseases, including inflammation, fibrosis and immune system diseases, and were also associated with some drugs, including prednisone, collagenase and mycophenolate mofetil, which may provide choice for treatment of UC. In conclusion, this study may provide novel insights into discovering potential molecular targets involved in the pathogenesis and treatment of UC.
溃疡性结肠炎(UC)是一种慢性炎症性肠病,与遗传和环境因素都有关;然而,UC 的潜在发病机制仍不清楚。本研究旨在通过全局生物信息学视角,进一步探讨从基因表达综合数据库中获得的 12 个 UC 患者的微阵列数据集,以探索 UC 的潜在遗传发病机制,包括差异表达基因(DEGs)的鉴定、功能富集、蛋白质-蛋白质相互作用、转录和转录后调控以及药物-基因关联。通过综合分析,筛选出 233 个 UC 与正常对照组织样本之间的差异表达基因;其中包括 173 个上调基因和 60 个下调基因。随后,发现 TATA 结合蛋白 1(TBP1;hsa_TATAAA_V$TATA_01)和核因子-κB(NF-κB;hsa_V$NFKAPPAB_01)等转录因子以及 microRNAs(miRNAs;如 miR-516-3p 和 miR-23a)与 233 个 DEGs 相关。值得注意的是,进一步分析表明,这些 DEGs 富集在某些疾病中,包括炎症、纤维化和免疫系统疾病,并且与一些药物(如泼尼松、胶原酶和霉酚酸酯)有关,这可能为 UC 的治疗提供选择。总之,本研究可能为发现 UC 发病机制和治疗的潜在分子靶标提供新的见解。