Fig 2: KSHV resolves the PROX1 bivalent chromatin by recruiting MLL2 and CFP1 and removing PRC2 to the PROX1 Promoter.Mock- and KSHV-infected PDLSCs were subjected to ChIP assay with antibodies against different histone methyltransferase components, including MLL1, MLL2, CFP1, UTX, RBBP5, WDR5, and EZH2 (a component of PRC2). Error bars represent SD. Statistics analysis was performed using the one-way ANOVA test. P-values < 0.05 were considered significant (*P<0.05, **P<0.01 and ***P<0.001) and N.S represents no significance.

Fig 3: The protein-protein interaction (PPI) network constructed using the STRING online database and Cytoscape software. A, The differentially expressed gene PPI network complex. The nodes denote proteins, and the edges denote the interaction of proteins. B-E, The clusters 1–4 for PPI were obtained by module analysis using the Cytoscape software (the degree of cutoff = 2, node score cutoff = 0.2, k-core = 2, and maximum depth = 100). The first 47 genes with high importance in the PPI network were screened out from B to E. They are IFI27, OASL, STAT1, IFI6, MMP1, MCM4, CHEK1, CCNE1, ISG15, RSAD2, TPX2, GBP1, TOP2A, KIF2C, PLAUR, SPP1, PLAU, CXCL12, CENPE, CDC20, MMP9, BST2, MKI67, CXCL8, CXCL1, IFI44, MMP13, IFI44 L, MMP3, TRIP13, COL14A1, COL7A1, COL1A2, COL4A5, COL5A2, COL4A2, ITGA6, COL4A6, COL4A1, TNC, APOL1, APP, SPARCL1, ADH1B, ALDH3A2, MAOB, and AOX1.

Fig 4: The prognostic information of the 47 core genes. Kaplan-Meier plotter online tools were used to identify the prognostic information of the 47 core genes and only 4 of 47 genes had a significantly worse survival rate (p < 0.05). HNSC: head-and-neck squamous cell carcinoma. A, The effect of SPP1 expression levels on HNSC patient survival. B, The effect of PLAU expression levels on HNSC patient survival. C, The effect of CXCL1 expression levels on HNSC patient survival. D, The effect of APP expression levels on HNSC patient survival.

Fig 5: Silencing of SPP1 suppresses migration, invasion, and the epithelial-to-mesenchymal transition (EMT) of tongue cancer cells. A, The detection of cell migration in tongue cancer using the scratch test. The scratch test was conducted on tongue cancer control cells as well as Si-RNA tongue cancer control and si-SPP1 SCC154 cells during the logarithmic phase of cell growth. The cell migration was measured 72 h later. The si-SPP1 cells had the longest migration distance and the strongest migration ability (p < 0.05). B, The Transwell assay for the invasive ability of SCC154 cells. The cells were cultured in a co-culture system and stained with a fluorescent dye after 36 h. The invasive ability of si-SPP1 SCC154 cells was stronger than that of normal SCC154 and Si RNA SCC154 cells (p < 0.05). C, Western blotting of EMT-related indicators of SCC154 cells. Western blotting was used to measure vimentin markers of the ability of the epithelial to stromal transformation of SCC154 cells in each group. The results showed that the expression of vimentin of si-SPP1 SCC154 cells was significantly lower than that of normal SCC154 and Si RNA SCC154 cells (p < 0.05). However, the expressions of E-cadherin and cytokeratin in si-SPP1 SCC154 cells were significantly higher than those in normal SCC154 and Si-RNA SCC154 cells (p < 0.05).