Yang Peng-Hui, Wei Ya-Nan, Xiao Bi-Juan, Li Si-Yi, Li Xin-Long, Yang Liang-Jun, Pan Hua-Feng, Chen Geng-Xin
The Second School of Clinical Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510006, Guangdong Province, China.
Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510006, Guangdong Province, China.
World J Gastrointest Oncol. 2024 Aug 15;16(8):3635-3650. doi: 10.4251/wjgo.v16.i8.3635.
Curcumin originates from the natural herb turmeric, and its antitumor effects have been known about for a long time. However, the mechanism by which curcumin affects gastric cancer (GC) has not been elucidated
To elucidate the potential mechanisms of curcumin in the treatment of GC.
Network pharmacological approaches were used to perform network analysis of Curcumin. We first analyzed Lipinski's Rule of Five for the use of Curcumin. Curcumin latent targets were predicted using the PharmMapper, SwissTargetPrediction and DrugBank network databases. GC disease targets were mined through the GeneCard, OMIM, DrugBank and TTD network databases. Then, GO enrichment, KEGG enrichment, protein-protein interaction (PPI), and overall survival analyses were performed. The results were further verified through molecular docking, differential expression analysis and cell experiments.
We identified a total of 48 curcumin-related genes with 31 overlapping GC-related targets. The intersection targets between curcumin and GC have been enriched in 81 GO biological processes and 22 significant pathways. Following PPI analysis, 6 hub targets were identified, namely, (), (), (), (), (), and (). These factors are correlated with decreased survival rates among patients diagnosed with GC. Molecular docking analysis further substantiated the strong binding interactions between Curcumin and the hub target genes. The experimental findings demonstrated that curcumin not only effectively inhibits the growth of BGC-823 cells but also suppresses their proliferation. mRNA levels of hub targets , , , and in BGC-823 cells were significantly increased in each dose group.
Curcumin can play an anti-GC role through a variety of targets, pathways and biological processes.
姜黄素源自天然草本植物姜黄，其抗肿瘤作用早已为人所知。然而，姜黄素影响胃癌（GC）的机制尚未阐明。
阐明姜黄素治疗GC的潜在机制。
采用网络药理学方法对姜黄素进行网络分析。我们首先分析了姜黄素的Lipinski五规则。使用PharmMapper、SwissTargetPrediction和DrugBank网络数据库预测姜黄素潜在靶点。通过GeneCard、OMIM、DrugBank和TTD网络数据库挖掘GC疾病靶点。然后，进行基因本体（GO）富集、京都基因与基因组百科全书（KEGG）富集、蛋白质-蛋白质相互作用（PPI）和总生存分析。通过分子对接、差异表达分析和细胞实验进一步验证结果。
我们共鉴定出48个与姜黄素相关的基因，其中31个与GC相关靶点重叠。姜黄素与GC之间的交集靶点已富集到81个GO生物学过程和22条显著通路中。经过PPI分析，确定了6个枢纽靶点，即（此处原文缺失具体靶点名称）。这些因素与GC诊断患者的生存率降低相关。分子对接分析进一步证实了姜黄素与枢纽靶基因之间的强结合相互作用。实验结果表明，姜黄素不仅能有效抑制BGC-823细胞的生长，还能抑制其增殖。BGC-823细胞中枢纽靶点（此处原文缺失具体靶点名称）的mRNA水平在各剂量组中均显著升高。
姜黄素可通过多种靶点、通路和生物学过程发挥抗GC作用。
