| Literature DB >> 33289330 |
Shuwei Zhang1, Chen Li1, Zhiying Zhang1, Yuchao Li1, Qian Li2, Fengxue Geng1, Junchao Liu1, Yaping Pan1,2.
Abstract
Accumulating evidence links Fusobacterium nucleatum with tumorigenesis. Our previous study demonstrated that F. nucleatum infection can induce epithelial-mesenchymal transition (EMT) in oral epithelial cells and elaborated a probable signal pathway involved in the induction of EMT. However, the comprehensive profiling and pathways of other candidate genes involved in F. nucleatum promoting malignant transformation remain largely elusive. Here, we analysed the transcriptome profile of HIOECs exposed to F. nucleatum infection. Totally, 3307 mRNAs (ǀLog2FCǀ >1.5) and 522 lncRNAs (ǀLog2FCǀ >1) were identified to be differentially expressed in F. nucleatum-infected HIOECs compared with non-infected HIOECs. GO and KEGG pathway analyses were performed to investigate the potential functions of the dysregulated genes. Tumour-associated genes were integrated, and top 10 hub genes (FYN, RAF1, ATM, FOS, CREB, NCOA3, VEGFA, JAK2, CREM and ATF3) were identified by protein-protein interaction (PPI) network, and Oncomine was used to validate hub genes' expression. LncRNA-hub genes co-expression network comprising 67 dysregulated lncRNAs were generated. Together, our study revealed the alteration of lncRNA and potential hub genes in oral epithelial cells in response to F. nucleatum infection, which may provide new insights into the shift of normal to malignant transformation initiated by oral bacterial infection.Entities:
Keywords: zzm321990Fusobacterium nucleatumzzm321990; TAGs; high-throughput sequencing; lncRNA; malignant transformation
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Year: 2020 PMID: 33289330 PMCID: PMC7812288 DOI: 10.1111/jcmm.16142
Source DB: PubMed Journal: J Cell Mol Med ISSN: 1582-1838 Impact factor: 5.295