转录组分析探讨揭示羊肚菌多糖ME-X抗S180肿瘤的分子机制  

Transcriptomes Analysis Revealed the Molecular Mechanism about the Anti-S180 Tumor Activity of the Polysaccharide ME-X from Morchella esculenta

作　　者：鲁艳 黄瑶[1] 叶姿妤 周丽倩 刘欣岚 丁祥 侯怡铃[1] LU Yan;HUANG Yao;YE Ziyu;ZHOU Liqian;LIU Xinlan;DING Xiang;HOU Yiling(Key Laboratory of Southwest China Wildlife Resources Conservation,Ministry of Education/College of Life Science,China West Normal University,Nanchong 637009,Sichuan,China;College of Environmental Science and Engineering,China West Normal University,Nanchong 637009,Sichuan,China)

机构地区：[1]西华师范大学生命科学学院/西南野生动植物资源保护教育部重点实验室,四川南充637009 [2]西华师范大学环境科学与工程学院,四川南充637009

出　　处：《四川农业大学学报》2022年第4期519-528,共10页Journal of Sichuan Agricultural University

基　　金：辐照保藏四川省重点实验室开放基金项目(FZBC2020009);四川省科技厅应用基础研究项目(2018JY0087);四川省科技厅重点研发项目(2018NZ0055)。

摘　　要：【目的】为探究羊肚菌多糖(ME-X)对S180肿瘤细胞抑制作用及其基因表达的影响,探索ME-X抑制小鼠S180肿瘤表型下潜在的作用分子及主要信号通路。【方法】以S180肿瘤小鼠为模型,先进行ME-X体内抑制小鼠S180肿瘤试验,再结合RNA-Seq测序技术对体内试验组中小鼠的S180肿瘤细胞进行测序并对得到的数据进行生物信息学分析。【结果】羊肚菌多糖(ME-X)和甘露聚糖肽(mannatide)一样能够极显著(P<0.01)抑制小鼠S180肿瘤的生长,其抑瘤率可达53.81%。差异表达基因(differential expressed genes,DEGs)分析结果显示羊肚菌多糖抑制S180肿瘤的关键基因主要富集在PI3K-AKT信号通路中,该通路中的成纤维细胞生长因子(Fgf10)、成纤维细胞生长因子受体(Fgfr2)、细胞因子受体(Prlr、Ghr、I12rb)、磷酸烯醇式丙酮酸羧激酶(Pck1)等多个基因显著上调。【结论】羊肚菌多糖(ME-X)可能通过PI3K-AKT信号通路调控S180肿瘤细胞代谢、迁移、细胞周期等进程达到抑制S180肿瘤的目的,为羊肚菌多糖抑制肿瘤分子机制研究提供可参考的理论依据。【Objective】This study aims to explore the antitumor activity of a polysaccharides from Morchella esculenta(named ME-X)and its impact on gene expression,observing the potential effect molecules and main signaling pathways under ME-X,which had a phenotype of suppressing the growth of S180 tumor in mice.【Method】In this study,the S180 tumor bearing mice were used as a model and antitumor experiments in mice were performed at first,then RNA-Seq technology was combined to sequence the S180 tumor cells from those mice in the experimental groups with bioinformatics analysis of the obtained data.【Result】ME-X,like Mannatide,which could significantly(P<0.01)inhibit the growth of S180 tumor in mice,and the rate of inhibition reached 53.81%.Differential expression genes(DEGs)analysis suggested that the key genes mostly enriched in the PI3K-AKT signaling pathway in‐cluding many significantly up-regulated genes,such as fibroblast growth factor 10(Fgf10),fibroblast growth factor receptor 2(Fgfr2),cytokine receptors(Prlr,Ghr,I12rb)and phosphoenolpyruvate carboxykinase(Pck1).【Conclusion】It was suggested that ME-X could regulate the metabolism,migration and cell cycle of S180 tumor cells through PI3K-AKT signaling pathway to inhibit S180 tumor.

关 键 词：羊肚菌多糖 S180肿瘤 RNA-SEQ 差异表达基因 PI3K-AKT信号通路 

分 类 号：Q591[生物学—生物化学]