GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.
State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Guangdong, China.
Biomed Res Int. 2021 Jul 19;2021:5521058. doi: 10.1155/2021/5521058. eCollection 2021.
Gastric cancer (GC) is the most common type of cancer. It is highly malignant and is characterized by rapid and uncontrolled growth. The antitumour activity of Baicalin was studied in multiple cancers. However, its mechanism of action has not been fully elucidated. We provided a systematic understanding of the mechanism of action of baicalin against GC using a transcriptome analysis of RNA-seq.
Human GC cells (SGC-7901) were exposed to 200 g/ml baicalin for 24 h. RNA-seq with a transcriptome, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were used to identify the antitumour effects of baicalin on SGC-7901 cells in vitro. A protein-protein interaction (PPI) network of differentially expressed genes (DEGs) was constructed. A competitive endogenous RNA (ceRNA) network was constructed and further analysed after validation using qRT-PCR.
A total of 68 lncRNAs, 20 miRNAs, and 1648 mRNAs were differentially expressed in baicalin-treated SGC-7901 GC cells. Three lncRNAs, 6 miRNAs, and 7 mRNAs were included in the ceRNA regulatory network. GO analysis revealed that the main DEGs were involved in the biological processes of the cell cycle and cell death. KEGG pathway analysis further suggested that the p53 signalling pathway was involved in the baicalin-induced antitumour effect on SGC-7901 cells. Further confirmation using qPCR indicated that baicalin induced an antitumour effect on SGC-7901 cells, which is consistent with the results of the sequencing data.
In summary, the mechanism of baicalin against GC involves multiple targets and signalling pathways. These results provide new insight into the antitumour mechanism of baicalin and help the development of new strategies to cure GC.
胃癌（GC）是最常见的癌症类型。它具有高度恶性，其特征是快速和不受控制的生长。黄芩苷已在多种癌症中进行了抗肿瘤活性研究。然而，其作用机制尚未完全阐明。我们使用 RNA-seq 的转录组分析，对黄芩苷治疗 GC 的作用机制进行了系统的了解。
将人 GC 细胞（SGC-7901）暴露于 200μg/ml 的黄芩苷中 24 小时。使用 RNA-seq 进行转录组、基因本体论（GO）和京都基因与基因组百科全书（KEGG）富集分析，以鉴定黄芩苷在体外对 SGC-7901 细胞的抗肿瘤作用。构建差异表达基因（DEG）的蛋白质-蛋白质相互作用（PPI）网络。构建竞争性内源 RNA（ceRNA）网络，并使用 qRT-PCR 进行验证后进一步分析。
黄芩苷处理的 SGC-7901 GC 细胞中共有 68 个 lncRNA、20 个 miRNA 和 1648 个 mRNA 表达差异。ceRNA 调控网络中包含 3 个 lncRNA、6 个 miRNA 和 7 个 mRNA。GO 分析表明，主要的 DEG 参与细胞周期和细胞死亡的生物学过程。KEGG 通路分析进一步表明，p53 信号通路参与了黄芩苷诱导的 SGC-7901 细胞抗肿瘤作用。使用 qPCR 进一步验证表明，黄芩苷对 SGC-7901 细胞具有抗肿瘤作用，这与测序数据的结果一致。
总之，黄芩苷对 GC 的作用机制涉及多个靶点和信号通路。这些结果为黄芩苷的抗肿瘤机制提供了新的见解，并有助于开发治疗 GC 的新策略。
