Exploration of Potential Targets and Mechanisms of Fisetin in the Treatment of Non-Small-Cell Lung Carcinoma via Network Pharmacology and In Vitro Validation.
Exploration of Potential Targets and Mechanisms of Fisetin in the Treatment of Non-Small-Cell Lung Carcinoma via Network Pharmacology and In Vitro Validation.
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通过网络药理学和体外验证探索非瑟酮治疗非小细胞肺癌的潜在靶点和机制
DOI：
10.1155/2022/2383527
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发表时间：
2022
影响因子：
--
通讯作者：
Zhang, Liang
中科院分区：
文献类型：
--
作者：
Ling, Junjun;Wang, Yuhong;Ma, Lihai;Chang, Aoshuang;Meng, Lingzhan;Zhang, Liang
目的非小细胞肺癌（non-small-cell lung cancer，NSCLC）的发病率和病死率较高，尽管采用多种治疗方法联合治疗。非瑟酮是一种小分子黄酮类化合物，具有抗肿瘤活性。因此，本研究旨在探讨非瑟酮治疗非小细胞肺癌的机制。方法采用TCMSP和Swiss target tools筛选非瑟酮的靶点，GeneCards收集NSCLC相关基因。通过Venn分析获得非瑟酮和NSCLC的共同基因，并对其可能的功能进行了进一步的注释。然后构建“化合物-靶标-疾病”网络，并过滤枢纽基因。此外，进行分子对接以预测非瑟酮与枢纽基因之间的结合能力。初步探讨非瑟酮对肺腺癌细胞hub基因表达的影响。结果共筛选出131个非瑟酮与NSCLC共有的基因，这些基因可能富集在抗氧化、细胞增殖、PI 3 K-Akt、IL-17等多种信号通路中。其中PIK 3R 1、CTNNB 1、JUN、EGFR和APP可能是中枢基因。分子对接表明非瑟酮与它们之间存在紧密的结合。实验提示非瑟酮可能对A549细胞中枢纽基因的表达有影响。结论本研究为非瑟酮治疗非小细胞肺癌提供了一系列新的靶点和途径。生物学过程涉及多个角度、多个靶点和多条途径，有待于进一步的实验验证。
Purpose The morbidity and fatality rates of non-small-cell lung cancer (NSCLC) were high, although a combination of multiple treatments was used. Fisetin, a small flavonoid compound, had shown anticancer activities. Thus, we aimed at exploring the mechanisms of Fisetin in the treatment of NSCLC. Methods TCMSP and Swiss target tools were used to screen the targets of Fisetin, and GeneCards was used to collect the genes related to NSCLC. The genes common to Fisetin and NSCLC were obtained by Venn analysis, whose possible functions were further annotated. A “Compound-Target-Disease” network was then constructed and hub genes were filtered. Also, molecular docking was performed to predict the binding abilities between Fisetin and the hub genes. Then, the effects of Fisetin on the expression of hub genes in lung adenocarcinoma cells were preliminarily evaluated in vitro. Results A total of 131 genes common to Fisetin and NSCLC were filtered out, which might be enriched in several biological processes including antioxidation, cell proliferation, and various signaling pathways, such as PI3K-Akt and IL-17 signaling pathways. Among them, PIK3R1, CTNNB1, JUN, EGFR, and APP might be the hub genes. Molecular docking indicated the close bond between Fisetin and them. Experiments implied a possible effect of Fisetin on the expression of hub genes in A549 cells. Conclusion The present study found a series of novel targets and pathways for Fisetin treating NSCLC. Multiple angles, targets, and pathways were involved in the biological processes, which need to be verified in further experiments.
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影响因子：
5.2
作者：
Rodak O;Peris-Díaz MD;Olbromski M;Podhorska-Okołów M;Dzięgiel P
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影响因子：
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作者：
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影响因子：
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作者：
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