Yang Sha, Huan Renzheng, Yue Jianhe, Guo Jin, Deng Mei, Wang Liya, Peng Shuo, Lin Xin, Liu Lin, Wang Jia, Han Guoqiang, Zha Yan, Liu Jian, Zhang Jiqin, Tan Ying
Guizhou University Medical College, Guiyang, Guizhou Province, China.
Department of Neurosurgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Front Pharmacol. 2023 Jan 20;14:1096159. doi: 10.3389/fphar.2023.1096159. eCollection 2023.
This study involved a multi-omics analysis of glioblastoma (GBM) samples to elaborate the potential mechanism of drug treatment. The GBM cells treated with or without orexin A were acquired from sequencing analysis. Differentially expressed genes/proteins/metabolites (DEGs/ DEPs/ DEMs) were screened. Next, combination analyses were conducted to investigate the common pathways and correlations between the two groups. Lastly, transcriptome-proteome-metabolome association analysis was carried out to determine the common pathways, and the genes in these pathways were analyzed through Kaplan-Meier (K-M) survival analysis in public databases. Cell and animal experiments were performed to investigate the anti-glioma activity of orexin A. A total of 1,527 DEGs, 52 DEPs, and 153 DEMs were found. Moreover, the combination analyses revealed that 6, 4, and 1 common pathways were present in the transcriptome-proteome, proteome-metabolome, and transcriptome-metabolome, respectively. Certain correlations were observed between the two data sets. Finally, 11 common pathways were discovered in association analysis, and 138 common genes were screened out in these common pathways. Six genes showed significant differences in terms of survival in both TCGA and CGGA. In addition, orexin A inhibited the proliferation, migration, and invasion of glioma and . Eleven common KEGG pathways with six common genes were found among different omics participations, revealing the underlying mechanisms in different omics and providing theoretical basis and reference for multi-omics research on drug treatment.
本研究对胶质母细胞瘤(GBM)样本进行了多组学分析,以阐明药物治疗的潜在机制。通过测序分析获得了用或不用食欲素A处理的GBM细胞。筛选出差异表达基因/蛋白质/代谢物(DEGs/DEPs/DEMs)。接下来,进行联合分析以研究两组之间的共同途径和相关性。最后,进行转录组-蛋白质组-代谢组关联分析以确定共同途径,并通过公共数据库中的Kaplan-Meier(K-M)生存分析对这些途径中的基因进行分析。进行细胞和动物实验以研究食欲素A的抗胶质瘤活性。共发现1527个DEGs、52个DEPs和153个DEMs。此外,联合分析显示转录组-蛋白质组、蛋白质组-代谢组和转录组-代谢组中分别存在6条、4条和1条共同途径。在两个数据集之间观察到一定的相关性。最后,在关联分析中发现了11条共同途径,并在这些共同途径中筛选出138个共同基因。六个基因在TCGA和CGGA中均显示出显著的生存差异。此外,食欲素A抑制胶质瘤的增殖、迁移和侵袭。在不同组学参与中发现了11条带有6个共同基因的KEGG共同途径,揭示了不同组学中的潜在机制,为药物治疗的多组学研究提供了理论依据和参考。