质粒蛋白pORF5通过MAPK/p38信号通路上调ZFAS1以促进宿主细胞存活。
Plasmid Protein pORF5 Up-Regulates ZFAS1 to Promote Host Cell Survival via MAPK/p38 Pathway.
作者信息
Wen Yating, Chen Hongliang, Luo Fangzhen, Zhao Lanhua, Shu Mingyi, Su Shengmei, Zhao Yuqi, Huang Qiulin, Li Zhongyu
机构信息
Institute of Pathogenic Biology, Hengyang Medical College, Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, China.
Department of General Surgery, First Affiliated Hospital of University of South China, Hengyang, China.
出版信息
Front Microbiol. 2020 Dec 17;11:593295. doi: 10.3389/fmicb.2020.593295. eCollection 2020.
Long non-coding RNAs (lncRNAs) have been demonstrated to play essential roles in many diseases. However, few studies have shown that lncRNAs take part in the pathogenesis of (). Here, we used a lncRNA microarray to detect the global lncRNA expression profiles in HeLa cells transfected with pORF5 plasmid protein, an important virulence factor for . The differentially expressed lncRNAs and mRNAs screened by microarray were selected for validation by quantitative real-time PCR. The up-regulated lncRNA zinc finger antisense 1 (ZFAS1) was presumed to involved in MAPK pathways by bioinformatics analysis. Inhibition of ZFAS1 decreased the apoptotic rate of pORF5 and reduced the infectivity of , and MAPK/p38 pathway was involved in anti-apoptotic effect induced by ZFAS1. Therefore, the present study confirmed that pORF5 up-regulates ZFAS1 to promote host cell survival via MAPK/p38 pathway and influences the infectivity of
长链非编码RNA（lncRNAs）已被证明在许多疾病中发挥重要作用。然而，很少有研究表明lncRNAs参与（）的发病机制。在此，我们使用lncRNA微阵列检测转染了pORF5质粒蛋白（一种重要的毒力因子）的HeLa细胞中的全局lncRNA表达谱。通过微阵列筛选出的差异表达lncRNAs和mRNAs通过定量实时PCR进行验证。通过生物信息学分析推测上调的lncRNA锌指反义1（ZFAS1）参与丝裂原活化蛋白激酶（MAPK）通路。抑制ZFAS1可降低pORF5的凋亡率并降低（）的感染性，且MAPK/p38通路参与ZFAS1诱导的抗凋亡作用。因此，本研究证实pORF5通过MAPK/p38通路上调ZFAS1以促进宿主细胞存活并影响（）的感染性
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