Fig 2: Overexpression and clinicopathological significance of ApoC3 in OSCC. (A,B) Flow cytometry analysis of the expression of ApoC3 in HIOEC and CAL27 cells. (C) Fluorescence confocal microscopy of the expression of ApoC3 in HIOEC and CAL27 cells. Scale bar, 10 µm. (D) Representative IHC staining of ApoC3 in oral mucosal tissue and OSCC tissue. Scale bar, 50 µm. (E) Quantitative analysis of ApoC3 expression in NOM, OED, and OSCC. (F) Representative IHC staining of ApoC3 in non-metastatic lymph node (LN−) and metastatic lymph node (LN+). Scale bar, 50 µm. (G) Quantitative analysis of ApoC3 expression in non-metastatic and metastatic lymph nodes. (H) Hierarchical clustering showing the correlation between ENO1 and ApoC3 in OSCC. (I) Correlation coefficient test of ENO1 with ApoC3 evaluated by Pearson’s analysis (p = 0.0479, r = 0.2966). * p < 0.05, ** p < 0.01, *** p < 0.001.

Fig 3: ENO1 induced proinflammatory cytokines in CAL27 supernatant and was dependent on ApoC3. (A) Western blot analysis for verifying ENO1 expression after control siRNA (ConsiRNA) and ENO1siRNA-1/2/3 transfection in CAL27 cells. (B) Heatmap of the production levels of the inflammatory cytokines in the cultured CAL27 cell supernatant, tested through a QAH-INF-1 cytokine antibody array. (C) Quantification of IL-8 production levels in the cultured CAL27 cell supernatant determined by the inflammatory cytokine assay. (D) Quantification of IL-8 production levels in the cultured CAL27 cell supernatant determined by ELISA. ** p < 0.01; ns is not significant. Each experiment was repeated at least three times.