Fig 1: Diagnostic efficiency of annexin V, CCT8, CFL1, ENO1, HSPB1, and TPM4 in diagnosing HCC in the test cohort comprised of normal healthy individuals (normal) and patients with HCC. (a) Comparison of the six protein expressions between 14 healthy individuals (normal) and 15 patients with HCC. (b) Area under the curve (AUC) and receiver operating characteristics (ROC) of six protein markers in diagnosing HCC. (c) Left panel: relative expression of CCT8 and CFL1 in serum exosomal mRNA of 29 healthy individuals (normal) and 20 patients with HCC. Right panel: area under the curve (AUC) and receiver operating characteristics (ROC) of serum exosomal CCT8 and CFL1 expression.
Fig 2: 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.
Fig 3: ENO1 directly bound to ApoC3 in postoperative lymphatic drainage (PLD) of metastatic OSCC. (A) Quantitative analysis of ENO1 expression in PLD between non-metastatic (left) and metastatic (right) OSCC patients. (B) The SDS-PAGE for the GST pulldown product shown by silver staining. (C) Western blot analysis using an anti-GST antibody for the GST pulldown product. (D) Distribution of the top 20 KEGG pathways based on ENO1-interacting proteins in PLD of metastatic OSCC. Columns refer to related pathways, which are colored with gradient colors from midnight red (metabolic pathways) to lighter red (central carbon metabolism in cancer). ** p < 0.01.
Fig 4: Overexpression and clinicopathological significance of ENO1 in primary oral squamous cell carcinoma (OSCC). (A) Representative immunohistochemical (IHC) staining of ENO1 in oral mucosal tissue and OSCC tissue. Scale bar, 50 µm. (B) Quantitative analysis of ENO1 expression in normal oral mucosa (NOM), oral epithelial dysplasia (OED), and OSCC tissues. (C) Quantitative analysis of ENO1 expression in OSCC classified by tumor sizes (T1, T2, T3, and T4). (D) Quantitative analysis of ENO1 expression in OSCC classified by tumor sizes (T1+T2, T3+T4). (E) Quantitative analysis of ENO1 expression in non-metastatic (left) and metastatic (right) OSCC tissues. (F) Representative IHC staining images of ENO1 in non-metastatic lymph node (LN-) and metastatic lymph node (LN+). Scale bar, 50 µm. (G) Quantitative analysis of ENO1 expression in non-metastatic and metastatic lymph nodes. * p < 0.05, *** p < 0.001; ns is not significant.
Fig 5: 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.
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